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Aim: There are very few studies in which retinopathy is determined by fundus fluorescein angiography (FFA) in prediabetics. We aimed to determine the frequency of retinopathy with a sensitive method and its relation to nephropathy in the prediabetic population. Materials and methods: We selected 30 impaired fasting glucose (IFG), 30 impaired glucose tolerance (IGT), and 30 IFG + IGT prediabetic patients, who were admitted to Ege University Faculty of Medicine between January 2019 and September 2019. Demographic and comorbidity profiles and laboratory data were collected. Microalbumin/creatinine ratio in spot urine was examined. FFA was performed in 86 eligible patients. Results: Sixteen (18.6%) of the 86 patients included in our study had very mild non-proliferative retinopathy according to FFA findings. Nephropathy was detected in 13 (15.1%) of 86 patients. Diabetic retinopathy (DR) was found to be significantly associated with age, systolic and diastolic blood pressure, serum uric acid level, estimated glomerular filtration rate (eGFR), and anti-hyperlipidemic drug use. A significant relationship was found between diabetic nephropathy and systolic blood pressure, serum uric acid levels, and eGFR levels. Conclusion: Our findings suggest the incidence of both retinopathy and nephropathy (18.6% and 15.1%, respectively) may be higher than expected in prediabetic patients. In addition, we describe that there may be a relationship between macrovascular complications and microvascular complications in patients with prediabetes. [ABSTRACT FROM AUTHOR]

Type 1 diabetes (T1D) is one of the most common chronic diseases in childhood, with a progressively increasing incidence. T1D management requires lifelong insulin treatment and ongoing health care support. The main goal of treatment is to maintain blood glucose levels as close to the physiological range as possible, particularly to avoid blood glucose fluctuations, which have been linked to morbidity and mortality in patients with T1D. Indeed, the guidelines of the International Society for Pediatric and Adolescent Diabetes (ISPAD) recommend a glycated hemoglobin (HbA1c) level < 53 mmol/mol (<7.0%) for young people with T1D to avoid comorbidities. Moreover, diabetic disease strongly influences the quality of life of young patients who must undergo continuous monitoring of glycemic values and the administration of subcutaneous insulin. In recent decades, the development of automated insulin delivery (AID) systems improved the metabolic control and the quality of life of T1D patients. Continuous subcutaneous insulin infusion (CSII) combined with continuous glucose monitoring (CGM) devices connected to smartphones represent a good therapeutic option, especially in young children. In this literature review, we revised the mechanisms of the currently available technologies for T1D in pediatric age and explored their effect on short- and long-term diabetes-related comorbidities, quality of life, and life expectation. [ABSTRACT FROM AUTHOR]

Kidney is a homeostasis organ in vertebrates involved in metabolizing and excreting molecules in the system. Diabetes is a known clinical disease characterized by persistent hyperglycemia, which induced oxidative stress. This study compared the effect of the extracts from scent (SLE), mentha (MLE), and thyme (TLE) leafy spices on blood glucose levels, renal purinergic enzymes [adenosine triphosphatase (ATPase), 5′-nucleotidase, and adenosine deaminase (ADA)], and antioxidant enzyme [glutathione transferase, superoxide dismutase, and catalase activities, and non-enzymatic antioxidant molecules [reactive species and thiol level in the pancreas tissue, and the level of urea, uric acid (AU), and creatinine in the serum of diabetic rats. Male (adult) Wistar rats were divided into nine (9) groups (n = 7). They were made diabetic with a single dose of 50 mg/kg STZ intraperitoneally (i.p.) except for the normal control group. Thereafter, the rats were administered with the studied extracts for 14 days. Blood glucose levels, renal purinergic enzymes, pancreatic antioxidant status, serum urea, uric acid (AU), and creatinine levels were determined. The study revealed that blood glucose levels and purinergic enzyme activities as well as kidney biomarkers in the serum were reduced, and that antioxidant enzyme activities and the level of thiols became better in renal extract-treated diabetic rats. Interestingly, it was observed that the 400 mg/mL TLE was more effective. In conclusion, the oral administration of extracts from the studied leafy spices could have beneficial effects against diabetic nephropathy. [ABSTRACT FROM AUTHOR]

Diabetes is the most frequent cause of kidney disease that progresses to end-stage renal disease worldwide, and diabetic kidney disease is significantly related to unfavorable cardiovascular outcomes. Since the 1990s, specific therapies have emerged and been approved to slow the progression of diabetic kidney disease, namely, renin–angiotensin–aldosterone system blockers (including angiotensin-converting enzyme inhibitors (ACEi) angiotensin receptor blockers (ARBs), the non-steroidal mineralocorticoid receptor antagonist (NS-MRA), finerenone, and sodium–glucose cotransporter-2 (SGLT2) inhibitors). Mechanistically, these different classes of agents bring different anti-inflammatory, anti-fibrotic, and complementary hemodynamic effects to patients with diabetic kidney disease such that they have additive benefits on slowing disease progression. Within the coming year, there will be data on renal outcomes using the glucagon-like peptide-1 receptor agonist, semaglutide. All the aforementioned medications have also been shown to improve cardiovascular outcomes. Thus, all three classes (maximally dosed ACEi or ARB, low-dose SGLT-2 inhibitors, and the NS-MRA, finerenone) form the "pillars of therapy" such that, when used together, they maximally slow diabetic kidney disease progression. Ongoing studies aim to expand these pillars with additional medications to potentially normalize the decline in kidney function and reduce associated cardiovascular mortality. [ABSTRACT FROM AUTHOR]

Background: Chronic pruritus is common in patients with diabetes though its pathophysiology is unknown and difficult to pinpoint given the multi‐system manifestations of diabetes. Herein, we aim to evaluate the severity of chronic itch in patients with diabetes and its association with glycaemic control, microvascular complications and quality of life. Methods: We conducted a retrospective study of 105 adults with diabetes evaluated by a dermatologist at a tertiary care centre in Mexico City. Degree of chronic pruritus and its impact on quality of life as well as laboratory, clinical and demographic data were collected. Patients without chronic pruritus (n = 62) were compared to those with chronic pruritus (n = 43). The latter cohort was further stratified by itch severity, and characteristics of their itch were quantified. Results: Neuropathy and loss of protective sensation were more common in patients with chronic pruritus, compared to those without chronic pruritus (p = 0.007 and p = 0.001, respectively). Anxiety and depression were more common in individuals with chronic pruritus (p = 0.009), and these group reported higher effect of pruritus on their quality of life (p < 0.0001). The most common sites of itch were the head, back and arms. Among patients with chronic itch, increasing itch severity was associated with decreasing eGFR (p = 0.080). Conclusions: The underlying cause of chronic itch in patients with diabetes is likely multifactorial and owing to microvascular complications such as neuropathy and nephropathy. Better understanding of the causes of itch in these patients can allow for more targeted treatment, leading to improved quality of life. [ABSTRACT FROM AUTHOR]

The kidney represents an important target of systemic inflammation. Its involvement in monogenic and multifactorial autoinflammatory diseases (AIDs) vary from peculiar and relatively frequent manifestations to some rare but severe features that may end up requiring transplantation. The pathogenetic background is also very heterogeneous ranging from amyloidosis to non-amyloid related damage rooted in inflammasome activation. Kidney involvement in monogenic and polygenic AIDs may present as renal amyloidosis, IgA nephropathy, and more rarely as various forms of glomerulonephritis (GN), namely segmental glomerulosclerosis, collapsing glomerulopathy, fibrillar, or membranoproliferative GN. Vascular disorders such as thrombosis or renal aneurysms and pseudoaneurysms may be encountered in patients with Behcet's disease. Patients with AIDs should be routinely assessed for renal involvement. Screening with urinalysis, serum creatinine, 24-h urinary protein, microhematuria, and imaging studies should be carried out for early diagnosis. Awareness of drug-induced nephrotoxicity, drug-drug interactions as well as addressing the issue of proper renal adjustment of drug doses deserve a special mention and should always be considered when dealing with patients affected by AIDs. Finally, we will explore the role of IL-1 inhibitors in AIDs patients with renal involvement. Targeting IL-1 may indeed have the potential to successfully manage kidney disease and improve long-term prognosis of AIDs patients. [ABSTRACT FROM AUTHOR]

In tropical countries, a mysterious tubulo-interstitial chronic renal disease (CKD), unrelated to diabetes, hypertension, and immunological causes, manifested four decades ago. Approximately 25,000 primarily middle-aged male farmers succumb annually to this crystal-tubular nephropathy (CTN). Without any known causative factors, it was identified as CKD of unknown aetiology (CKDu). Because multiple factors contribute to causing it later, was changed to CKD of multi-factorial (CKDmfo). Despite no evidence, it was hypothesised to cause by agrochemicals or heavy metals in food or drinking contaminated water. However, current data suggest that the CKD-CTN is due to natural geogenic water contamination. Consumption of concentrated stagnant groundwater from deep-dug wells and tube wells containing hard water and fluoride, overdecades is necessary for its clinical manifestations. In all affected countries have prolonged annual dry seasons that led to the evopo-concentration of ions and minerals in groundwater, making hard water even more unpalatable, thus, peasants consume lesser amounts of water. They develop chronic dehydration from daily exposure to hot climatic conditions aggravated by regular alcohol intake. These conditions provide a highly conducive environment—a perfect storm for calcium phosphate (CaPO4) crystal formation in renal tissues. Our recent histological and preliminary electron microscopic data reveal deposition of CaPO4 crystals and nano-tubes in kidneys. While CaPO4 nano-minerals are unstable, the presence of fluoride ions stabilises and allows their growth. This new concept paves the path for highly cost-effective, straightforward local solutions to protect farm workers and eliminate the disease, without embarking on expensive medications, interventions, or building hospitals. Chronic dehydration-associated CKD–CTN is preventable by increased consumption of potable water. Increasing clean water consumption reduces CKD–CTN incidence, and associated morbidities and premature deaths. However, the damage becomes irreversible when the disease advances beyond CKD stage IIIB. The incidence of this deadly renal failure can be prevented by its education, lifestyle changes, and increased water consumption, not by treating the renal disease or expanding dialysis centres/hospitals, or transplantation services. Eradication of CKD-CTN cost significantly less than the current approach of treating affected persons and unnecessarily expanding health infrastructure. Since the manifestation of CKD-CTN is due to consuming naturally contaminated drinking water (with calcium containing hard water and fluoride), it is not difficult to remove these to prevent CKD-CTN: thus, international assistance is unwarranted for its eradication. The straightforward approaches described here will prevent CKD–CTN and save thousands of lives in affected farming communities. Keypoints: During the past four decades, an unusual tubulointerstitial chronic renal disease (CKD) unrelated to diabetes, hypertension, or immunological causes, manifested in over twenty tropical countries located north of the equator. Previously, this crystal-tubular nephropathy (CKD–CTN) was assumed to arise from agrochemical or heavy metal contamination. Natural geogenic conditions/events contaminate groundwater. Drinking such concentrated, stagnant groundwater in the presence of chronic dehydration over a prolonged period leads to the development of CKD–CTN. Nano-minerals stabilised with fluoride ions grow perniciously in kidney tissues in the presence of dehydration. It provides a conducive environment for CaPO4 crystal formation in renal tubules and interstitial tissues. In conjunction with lifestyle changes and providing affordable clean drinking water will prevent the disease and eventually eradicate CKD–CTN. Those with CKD stages below stages IIIB can reverse by drinking plenty of clean water. These approaches would save thousands of lives in affected communities and healthcare costs. [ABSTRACT FROM AUTHOR]

Objective: Diabetic nephropathy is one of the most important complications in diabetes mellitus. We aimed to examine the influence of organ-specific antibody seropositivity in diabetic nephropathy. Methods: Patients with type 1 diabetes and no evidence of celiac disease, thyroid dysfunction, and other kidney diseases and with an annual average HbA1c level <10%, body mass index <25 kg/m2, and normal blood pressure were enrolled. Results: Eighty patients (39 boys and 41 girls) were evaluated. Twenty patients with moderately increased albuminuria (diabetic nephropathy group) and 60 patients without albuminuria (control group) showed no statistical difference in age, gender, diabetes duration, age at diagnosis, kidney function tests, and mean blood pressure measurements. Compared to control group, the mean anti-thyroglobulin level and anti-thyroxin peroxidase level were statistically higher in the diabetic nephropathy group, P = .004 and P = .045, respectively. However, the thyroid function tests were normal in either group. Conclusion: Determination of the impact of autoantibody seropositivity on the risk of diabetic nephropathy in type 1 diabetic children could be a non-traditional marker in the risk assessment of diabetic nephropathy [ABSTRACT FROM AUTHOR]

Key Clinical Message: There may be a connection between pemphigus vulgaris and nephrotic syndrome, as evidenced by the occurrence of focal segmental glomerulosclerosis in our pemphigus vulgaris patient and reviewing relevant literature. Therefore, if a patient with pemphigus vulgaris presents with bilateral lower extremity edema or proteinuria detected during urinalysis, it could indicate involvement of the kidneys. Pemphigus vulgaris is a type of autoimmune blistering disease characterized by the presence of IgG autoantibodies against desmogleins 3 and 1. It is important to evaluate potential autoimmune associations in patients with pemphigus vulgaris so that appropriate laboratory and physical examinations can be performed to monitor for any increased risk of other autoimmune disorders. This case report describes a 55‐year‐old woman who presented with oral and axillary erosions, which were diagnosed as pemphigus vulgaris based on skin histopathology and immunofluorescence. During follow‐up, the patient was found to have proteinuria, which led to referral to a nephrologist. The patient was diagnosed with nephrotic syndrome and minimal change disease after a biopsy. Despite treatment, the patient's proteinuria persisted and serum creatinine levels increased, leading to a second biopsy which confirmed the diagnosis of focal segmental glomerulosclerosis. This study reports on the first case of pemphigus vulgaris with focal segmental glomerulosclerosis and reviews the literature on the co‐occurrence of acquired immunobullous diseases and nephrotic syndrome of any kind. [ABSTRACT FROM AUTHOR]

Background: One of the leading causes of kidney failure in people living with HIV is HIV-associated nephropathy (HIVAN), the first form of renal involvement in HIV patients to be described. Objective: Review of literature about Human Immunodeficiency Virus Infection Associated Nephropathy. Methods: We searched PubMed, Google Scholar, and Science Direct for relevant articles on Human Immunodeficiency Virus, and Nephropathy. Only the most recent or thorough studies were taken into account between December 1981 and January 2020. The authors also evaluated the value of resources culled from other works in the same genre. Therefore, documents written in languages other than English have been ignored due to a lack of translation funds. Unpublished works, oral presentations, conference abstracts, and dissertations were generally agreed upon not to be qualified as scientific research. Conclusion: According to reports, roughly 20% of HIV-infected people have end-stage renal disease, making it the third leading cause of such disease among African-Americans aged 20 to 64 years old. Some parts of Africa, for example, where the reduction is not as pronounced possibly due to a lack of antiretroviral treatment availability, are typical of such communities. The classic manifestation of HIVAN is known as collapsing glomerulopathy, and it is accompanied by proteinuric nephrotic syndrome, tubulointerstitial involvement, characterized by the enlargement and production of tubular microcysts as well as interstitial inflammation and tubular damage, Its symptoms could include blood in the urine (hematuria), quickly progressing kidney failure, and high blood pressure in the arteries. [ABSTRACT FROM AUTHOR]

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Immunoglobulin A nephropathy (IgAN) is characterized by mesangial deposition of immune complexes containing galactose-deficient IgA1 (Gd-IgA1). This Gd-IgA1 is believed to originate from mucosally sited B cells, which are abundant in the Peyer's patches-rich distal ileum. Nefecon is a targeted-release form of budesonide developed to act in the distal ileum, thereby exerting a direct action on the mucosal tissue implicated in the pathogenesis of the disease. This review discusses IgAN pathophysiology and provides an overview of the current therapeutic landscape, focusing on Nefecon, the first drug to receive accelerated US approval and conditional EU approval for the treatment of patients with IgAN at risk of rapid disease progression. Nefecon trial data thus far have demonstrated a promising efficacy profile, with a predictable pattern of adverse events. Treatment with Nefecon for 9 months reduces proteinuria substantially (Part A of the Phase 3 trial and the Phase 2b trial). A nearly complete prevention of deterioration of renal function has been observed at 12 months in patients at greatest risk of rapid disease progression. Long-term data from Part B of the Phase 3 study will provide 24-month data, furthering understanding of the durability of the 9-month treatment course. [ABSTRACT FROM AUTHOR]

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Over the past 30 years, climate change has taken one of the leading places among the ten main causes of death due to natural disasters. Rising temperatures have been shown to increase emergency department admissions for a wide range of kidney diseases, including acute kidney injury (AKI), chronic kidney disease, kidney stones, and urinary tract infections. The occupational effect of heat stress is also associated with AKI, which can quickly progress to acute kidney failure with high mortality. The basis of the pathogenetic mechanisms of heat-induced AKI is a decrease in the circulating blood volume and electrolyte disturbances due to increased perspiration. Water evaporation from the surface of the skin contributes to dehydration with an increase in serum osmolarity. In response to this, vasopressin is activated, the specific gravity of urine increases, and the amount of urine decreases. The glomerular filtration rate progressively decreases. Hypokalemia develops, which changes to hyperkalemia within 12 hours. Tubular endothelium is damaged, which leads to microthrombosis of afferent and efferent renal arteries, the development of an inflammatory response, and exhaustion of the renal interstitium. Possible rhabdomyolysis and myoglobinemia with subsequent tubular obstruction worsen existing kidney damage. According to the leading mechanism of damage, there are two types of acute heat damage to the kidneys: classical rhabdomyolysis and acute interstitial nephritis. Although modern medical advances have contributed to the development of effective treatment and management strategies (rapid cooling, extracorporeal detoxification methods, etc.), mortality in kidney damage due to general overheating has decreased slightly over the past decades. For health care and industry researchers, it is necessary to identify the harmful occupational conditions that lead to heat stress nephropathy and to develop certain occupational safety strategies. [ABSTRACT FROM AUTHOR]

Oxalate nephropathy, due to secondary hyperoxaluria has widely been described in gastrointestinal diseases. However, reports of oxalate nephropathy in newly diagnosed celiac disease are rare. A 72-year-old Caucasian male presented to the hospital with abdominal discomfort and acute renal insufficiency with a creatinine of 290 µmol/L. The clinical course, laboratory results and urinalysis were suspect for tubular injury. Renal biopsy showed calcium oxalate depositions. Elevated plasma and urine oxalate levels established the diagnosis oxalate nephropathy. The abdominal complaints with steatorrhea and positive anti-tissue transglutaminase antibodies were diagnosed as celiac disease, which was confirmed after duodenal biopsies. Treatment with prednisone, and gluten-free, low oxalate and normal calcium diet, lowered the plasma oxalate levels and improved his renal function. Decreased absorption of free fatty acids can lead to increased free oxalate in the colon due to the binding of free fatty acids to calcium, preventing the formation of the less absorbable calcium oxalate in the colon. Oxalate dispositions in the kidney can lead to acute tubular injury and chronic renal insufficiency. Celiac disease is therefore one of the intestinal diseases that can lead to hyperoxaluria and oxalate nephropathy. [ABSTRACT FROM AUTHOR]

Fabry disease (FD) is a rare genetic disorder caused by a deficiency in the α-galactosidase A enzyme, which results in the globotriaosylceramide accumulation in many organs, including the kidneys. Nephropathy is a major FD complication that can progress to end-stage renal disease if not treated early. Although enzyme replacement therapy and chaperone therapy are effective, other treatments such as ACE inhibitors and angiotensin receptor blockers can also provide nephroprotective effects when renal damage is also established. Recently, SGLT2 inhibitors have been approved as innovative drugs for treating chronic kidney disease. Thus, we plan a multicenter observational prospective cohort study to assess the effect of Dapagliflozin, a SGLT2 inhibitor, in FD patients with chronic kidney disease (CKD) stages 1–3. The objectives are to evaluate the effect of Dapagliflozin primarily on albuminuria and secondarily on kidney disease progression and clinical FD stability. Thirdly, any association between SGT2i and cardiac pathology, exercise capacity, kidney and inflammatory biomarkers, quality of life, and psychosocial factors will also be evaluated. The inclusion criteria are age ≥ 18; CKD stages 1–3; and albuminuria despite stable treatment with ERT/Migalastat and ACEi/ARB. The exclusion criteria are immunosuppressive therapy, type 1 diabetes, eGFR < 30 mL/min/1.73 m2, and recurrent UTIs. Baseline, 12-month, and 24-month visits will be scheduled to collect demographic, clinical, biochemical, and urinary data. Additionally, an exercise capacity and psychosocial assessment will be performed. The study could provide new insights into using SGLT2 inhibitors for treating kidney manifestations in Fabry disease. [ABSTRACT FROM AUTHOR]

Prognosis of hypertension leads to organ damage by causing nephropathy, stroke, retinopathy and cardiomegaly. Kidney, retinopathy and blood pressure (BP) have been discussed in plenty in relation with catecholamines of autonomic nervous system (ANS) and angiotensin II of renin angiotensin aldosterone system but very little have been told about the role of endocannabinoid system (ECS) in the regulation of kidney function, retinopathy and BP. ECS is a unique system in the body, which can be considered as master regulator of body functions. It encompasses endogenous production of its cannabinoids, its degrading enzymes and functional receptors, which innervate and perform various functions in different organs of the body. Kidney, retinopathy and BP pathologies arise normally due to elevated catecholamine and ang II, which are vasoconstrictor in their biological nature. Question arise which system or agent counterbalances the vasoconstrictors effect of noradrenaline and ang II in normal individuals? This review will not only try to illustrate the significance of ECS in the kidney and BP regulation but also establish the connection of ECS with ANS and ang II. This review will also explain that ECS, which is vasodilator in its action either independently counteract the effect produced with the vasoconstriction of ANS and ang II or by blocking some of the common pathways shared by ECS, ANS, and ang II in the regulation of kidney and BP regulation. This article conclude that persistent control of BP and normal functions of kidney is maintained either by decreasing systemic catecholamine, ang II or by up regulation of ECS, which will result in the regression of nephropathy, stroke, retinopathy, and cardiomegaly induced by hypertension. [ABSTRACT FROM AUTHOR]

An elderly woman with preinvasive breast cancer, atrial fibrillation, coronary artery-pulmonary artery fistula, pulmonary hypertension and Stage 4 diabetic nephropathy underwent a mastectomy and sentinel lymph node biopsy. Managing her perioperative fluid balance and anticoagulation treatment were challenging. Having a malignancy, atrial fibrillation plus underhydration will increase her risk of hypercoagulation. However, fluid overload will lead to pulmonary oedema which will decrease her oxygenation further in pulmonary hypertension. Cessation of anticoagulation also increased the risk of hypercoagulation. Anticoagulant therapy increases the risk of a perioperative wound haematoma, which may require another general anaesthesia for identification and arrest of the bleeding source and haematoma evacuation. A haematoma will also increase the risk of surgical site infection; especially as a diabetic. Her anticoagulant therapy (rivoroxaban) was stopped four days preoperatively. Her ejection fraction was 50%, with Grade II diastolic dysfunction and TAPSE 0.6 cm. Her CHA2DS2-VASc Score was 5. Perioperatively, intraarterial cannulation was connected to the FloTrac™ sensor and EV1000™ monitor. Her fluid management was monitored using goal directed (GD) fluid therapy. The patient underwent surgery successfully and her anticoagulant therapy was recommenced 14 days postoperatively. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Taibah University Medical Sciences is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: In Fabry Disease (FD), although the primary factor initiating kidney damage is glycosphingolipid accumulation, secondary conditions such as increased inflammation and fibrosis may cause this damage to progress. These processes may be induced by immune cells. Therefore, we aimed to investigate the peripheral lymphocyte subgroup analysis of the patients with FD and compare these results with healthy individuals. In addition, we performed T, B, NK, and plasma cell analyses in kidney biopsy materials and compared these kidney biopsy results with the biopsy results of patients whose kidney functions were impaired after 4 years of regular ERT. Materials and methods: 18 FD and 16 healthy individuals were included in the study. T-B lymphocyte and NK-cell populations were determined. We performed kidney biopsies (KBx) on 13 patients with FD prior to ERT. Of these, 4 patients had rebiopsy after 4 years of regular ERT. Immunohistochemical staining was performed to define immune cell infiltration. Results: There was no statistically significant difference in terms of total, helper and cytotoxic T-lymphocyte and CD3−CD16+CD56+ natural killer (NK)-cell count (p = 0.20; p = 0.12; p = 0.76; p = 0.75, respectively).According to KBx findings prior to ERT, all patients had interstitial fibrosis (IF), podocyte vacuoles (PV), and podocyte inclusion (PI), CD3, CD4, CD8, CD16, and CD56 positivity at different levels. None of the patients had CD19, CD20, and CD138 positivity at the first biopsies. When we compared the first and the second KBx results of the two progressors, we also demonstrated that CD3+4+T-cells infiltration remained the same, whereas CD8+T cells, CD16+ and 56+NK-cells infiltration were significantly decreased. In contrast, CD20+B cells and CD138+plasma cell infiltration were significantly increased despite 4 years of ERT (15 fold and sixfold, respectively). The CD20+B and CD138+ plasma cells and IF were positively correlated with proteinuria. Conclusions: The progression of FD nephropathy and proteinuria is increased despite a long-term ERT. Immune cells, primarily B and plasma cells, might cause these unwanted consequences. [ABSTRACT FROM AUTHOR]

Rationale & objectiveAPOL1 nephropathy risk alleles are associated with the development of chronic kidney disease (CKD) in African Americans. Although CKD is an established risk factor for mortality, associations of APOL1 risk alleles with mortality are uncertain.Study designProspective cohort.Settings & participants10,380 African American and 17,485 white American participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study.ExposuresAPOL1 nephropathy risk alleles.OutcomesAll-cause and cause-specific mortality.Analytical approachCox proportional hazards models were used to examine the association of APOL1 high-risk genotypes (2 risk alleles) versus APOL1 low-risk genotypes (0/1 risk allele) with all-cause and cause-specific mortality in African Americans and examine the risk for all-cause mortality in African Americans with high-risk genotypes versus African Americans with low-risk genotypes and white Americans.ResultsAPOL1 high-risk participants were younger and had a higher prevalence of albuminuria than low-risk participants. There was no statistically significant association of APOL1 high- versus low-risk genotypes with all-cause mortality in models adjusted for sociodemographic variables, comorbid conditions, and kidney function (HR, 0.88; 95% CI, 0.77-1.01). After further adjustment for genetic ancestry in a subset with available data, a statistically significant association emerged (HR, 0.81; 95% CI, 0.69-0.96). Associations differed by CKD status (Pinteraction=0.04), with African Americans with high-risk genotypes having lower risk for mortality than those with low-risk genotypes in fully adjusted models (HR, 0.78; 95% CI, 0.62-0.99) among those with CKD, but not those without CKD (HR, 0.84; 95% CI, 0.66-1.05). Compared with white Americans, African Americans with high-risk genotypes had a similar rate of mortality, whereas African Americans with low-risk genotypes had a higher rate of mortality (HR, 1.07; 95% CI, 1.00-1.14) in fully adjusted models.LimitationsLack of follow-up measures of kidney function.ConclusionsAfrican Americans with high-risk APOL1 genotypes had lower mortality than those with low-risk genotypes in multivariable-adjusted models including genetic ancestry.

Background. The early onset of nephropathies creates certain risk of early chronic kidney disease development with loss of function (especially in children with unfavorable intrauterine period), renal tissue dysplasia, congenital malformations and/or urodynamic disorders.Objective. The aim of the study is to evaluate the role of ontogenesis factors in nephropathies development in tender-age infants with specification of the course features and kidneys morphometric parameters.Methods. Cohort study was conducted. The study group included 69 children aged from 0 to 36 months with changes in the kidneys (compared to age-specific ones) according to ultrasound and/or urinary syndrome (leukocyturia, bacteriuria, proteinuria, etc.). The control group included 35 relatively healthy children of the same age. Comparative analysis of antenatal and postnatal medical history was carried out in both groups, as well as comparison of morphometric indicators of the urinary system organs at neonatal ultrasound screening. Pathological process onset was also considered in the group of children with nephropathies. The study was conducted during 2018–2021.Results. Possible predictors of pathology process in children with early onset of nephropathies are: 1) maternal diseases: urinary system disorders (OR = 4.99), blood pathology, mainly anemia of the 2nd–3rd grade (OR = 6.94), cardiovascular system diseases (OR = 10.26), inflammatory diseases of genital tract (OR = 10.61); 2) pregnancy failures: gestational diabetes mellitus (OR = 7.24), preeclampsia and eclampsia (OR = 4.40); placental pathology (OR = 17.0), and fetoplacental insufficiency (OR = 7.61); 3) feeding features: early conversion to breast-milk substitutes (OR = 2.81). 50.7% of children of this group has shown persistent urodynamic disorders already at first months of life according to ultrasound data, as well as signs of bloated kidneys. It was shown that the inflammatory process manifestation associated with aggravated perinatal history and congenital defects occurs significantly earlier — 2 months, and without any defects — 4 months (p = 0.004).Conclusion. Burdened antenatal and neonatal medical history has negative effect on the morphogenesis of the urinary system organs and creates conditions for early nephropathies development during the first months of life.

The incidence of diabetes is increasing worldwide, emphasizing an emerging need for blood glucose control optimization to prevent the development of chronic complications and improve the quality of life. This retrospective cohort study aimed to investigate the effects of total physical activity on microvascular diabetic complication development in patients with type 1 diabetes mellitus (T1DM). The study included 71 T1DM patients, average age 41 years and HbA1c 7.78%. Most patients (82.1%) reported having hypoglycemia, while the minority of patients developed microvascular complications, mostly nonproliferative retinopathy (17.7%). All subjects included in the study were moderately or vigorously physically active. No association was observed between total physical activity and regulation of glycemia, hypoglycemic incidents, or development of microvascular complications. Until sufficient data from prospective studies become available, our data support the findings of no negative effect of higher intensity physical activity on the development of microvascular complications in T1DM patients.

Background: Diabetic nephropathy (DN) accounts for the most prevalent cause of chronic kidney disease and end-stage renal disease (ESRD) globally, accounting for about 50% of all ESRD patients that need management with dialysis or a renal transplant. Objectives: The aim of this study was to the role of Asprosin as an independent and trustworthy biomarker for the quick diagnosis of DN by knowing the sensitivity and specificity, acceptable to add to the diagnostic protocol. Evaluated fasting blood glucose asprosin, lipid profile, urea, creatinine, and albumin levels in apparently healthy groups, diabetic groups, and diabetic groups with nephropathy to determine their medical significance; asprosin can be used as an independent and trustworthy biomarker for the quick diagnosis of DN by knowing the sensitivity and specificity, acceptable to add to the diagnostic protocol. Materials and Methods: Blood samples were obtained from the Diabetes and Endocrine Center in Hilla city, Babylon province’s Marjan Medical City, from October 25, 2021 to January 31, 2022. Sixty type 2 diabetes mellitus (T2DM) patients were classified into 30 with diabetes mellitus, 30 with DN, and 30 apparently healthy patients. Serum asprosin levels were measured using a commercial enzyme-linked immunosorbent assay kit. SPSS software was used to conduct the statistical analysis. Results: Both T2DM patients with and without nephropathy had considerably higher levels of fasting blood glucose (FBG), asprosin, serum urea, creatinine, total cholesterol, triglyceride (TG), low-density lipoprotein cholesterol, and very low-density lipoprotein cholesterol compared to the healthy appearance group, although both groups had significantly lower levels of albumin and high-density lipoprotein cholesterol (HDL-C). Asprosin additionally showed a positively correlated with serum urea, TG, and HDL-C and shown negative correlation with serum albumin. The sensitivity and specificity of the test at the cut-off value of asprosin 17.5 ng/mL were 86.7% and 80%, respectively, and the area under the curve was 0.92, P-value = 0.001. Conclusion: Because blood asprosin levels have a sensitivity and specificity of more than 80% in T2DM patients with nephropathy, they can be used as an independent and trustworthy biomarker for the quick diagnosis of DN.

Mesenchymal stem cells (MSCs) can reduce inflammation, restore renal injury and maintain immune homeostasis by paracrine various cytokines and regulating immune cells. In preclinical studies, it has been proved that mesenchymal stem cells have obvious therapeutic effects on acute kidney injury, diabetic nephropathy, lupus nephritis and various glomerular diseases in animal models. In clinical studies, mesenchymal stem cells have also been shown to be safe and partially effective. Mesenchymal stem cell therapy has revealed a new model of biotherapy in kidney diseases.

Introduction: Chronic kidney disease (CKD) affects every organ system including the eye. Aim: To conduct a thorough ocular examination in the patients of CKD and to analyse the findings. Materials and Methods: A total of 100 cases were collected from the nephrology unit of our tertiary centre. This was a cross-sectional, hospital-based study. Results: The commonest causes for visual impairment were maculopathy followed by cataracts. The other ocular findings were progressive pterygium, keratitis, central retinal vein occlusion (CRVO), retinal detachments (RDs), vitreous haemorrhage (VH) and disc-related changes. Hypertensive retinopathy (HR) was more prevalent and tended to be more severe as the renal disease progressed. More severe grades of diabetic retinopathy (DR) were detected with increasing severity of the renal disease. Conclusion: This study shows the importance of ocular evaluation of patients with CKD.

Background: The causal association between IgA nephropathy (IgAN) and celiac disease (CeD) is based on their clinical coexistence. In this prospective study, we screened patients with IgAN for CeD and explored the utility of analysis of IgA anti-TG2 antibody deposits, for establishing a causal association. Methods: Biopsy-proven patients of IgAN were screened for serum IgA anti-tissue transglutaminase antibody (IgA anti-tTG Ab) titer and thereafter were invited to undergo endoscopic duodenal biopsy. Corresponding duodenal and kidney biopsies were subjected to IgA anti-TG2 antibody colocalization study using dual-color immunohistochemistry and immunofluorescence techniques. Additionally, kidney biopsies from 105 patients with IgAN who did not give consent for serology analysis, 30 non-IgA nephropathies, and 10 normal controls were also included. Dual-color-stained slides were interpreted based on stain distribution and intensity scores, and Pearson's index >0.3–1 on confocal imaging was considered significant. Results: Of a cohort of 151 patients with IgAN, 32 consented to undergo sero-screening and 5 of them had high serum anti-tTG Ab titer. Two out of the latter consented to endoscopic duodenal biopsies, in whom modified Marsh grade 3b changes were identified. Strong IgA anti-TG2 antibody deposits were noted in the kidney and duodenal biopsies of these patients. One patient out of non-consenting 105 patients with IgAN and 3 out of 30 patients with other non-IgA nephropathies also showed IgA anti-TG2 deposits. None of the healthy kidney tissues showed IgA anti-TG2 Ab deposits. Conclusions: Co-localized IgA anti-TG2 deposits in the kidney biopsies in patients with IgAN help to establish a pathogenic link with CeD. A small proportion of patients with IgAN have associated CeD.

Abstract Background Schimke immunoosseous dysplasia (SIOD) is an ultra-rare inherited disease affecting many organ systems. Spondyloepiphyseal dysplasia, T-cell immunodeficiency and steroid resistant nephrotic syndrome are the main symptoms of this disease. Case presentation We aimed to characterize the clinical, pathological and genetic features of SIOD patients received at tertiary Pediatric Nephrology Center, University Hospital Motol, Prague, Czech Republic during the period 2001–2021. The mean age at diagnosis was 21 months (range 18–48 months). All patients presented with growth failure, nephropathy and immunodeficiency. Infections and neurologic complications were present in most of the affected children during the course of the disease. Conclusions Although SIOD is a disease characterized by specific features, the individual phenotype may differ. Neurologic signs can severely affect the quality of life; the view on the management of SIOD is not uniform. Currently, new therapeutic methods are required.

Abstract Background Type 2 diabetes mellitus (T2DM) approximately constitutes 90% of the reported cases. 30-40% of diabetics eventually develop diabetic nephropathy (DN); accounting for one of the major causes of morbidity and mortality. Increased glucose autoxidation and non-enzymatic glycation of proteins in diabetic kidneys lead to the excessive generation of reactive oxygen species (ROS) that results in lipid peroxidation and activation of inflammatory mediators which overwhelms the scavenging capacity of the antioxidant defense system (Nrf2/Keap1/HO-1). Centratherum anthelminticum commonly called as kali zeeri (bitter cumin) and its seeds are well known for culinary purposes in Asia (Pakistan). It has reported anti-inflammatory, antioxidant, and anti-diabetic activities. The present study has attempted to explore the in-vivo anti-inflammatory, antioxidant and antihyperglycemic potential of the C. anthelminticum seed’s fixed oil (FO) and its fractions in high fat-high fructose-streptozotocin (HF-HFr-STZ) induced T2DM rat model. Methods The T2DM rat model was developed by giving a high-fat and high-fructose diet followed by a single intraperitoneal injection of streptozotocin (STZ 60 mg/kg) on 28th day of the trial. After 72 hours of this injection, rats showing fasting blood glucose (FBG) levels≥230 mg/dL were recruited into six groups. These groups were orally administered distilled water (1 mL/kg), Gliclazide (200 mg/kg), Centratherum anthelminticum seed (FO) and its hexane (HF), chloroform (CF) and ethanol (EF) soluble fractions (200 mg/kg each), respectively for 4 weeks (i.e. 28 days). Blood, serum, and kidney tissue samples of euthanized animals were used for biochemical, pro-inflammatory, and antioxidant markers (ELISA, qRT-PCR, and spectrophotometric assays) and histology, respectively. Results C. anthelminticum FO and its fractions reduced the lipid peroxidation, and improved the antioxidant parameters: enzymatic (SOD, CAT, and GPx), non-enzymatic (GSH), and mRNA expression of anti-inflammatory markers (Nrf-2, keap1, and HO-1). mRNA expression of inflammatory and apoptotic markers (TNF-α, IL-1β, COX-1, NF-κB, Bax, and Bcl-2) were attenuated along with improved kidney architecture. Conclusion C. anthelminticum can mitigate inflammation and oxidative stress in early DN. The anti-nephropathic effect can be attributed to its ability to down-regulate NF-κB and by bringing the Nrf-2 expression levels to near normal.

Objective(s): Accumulation of methylglyoxal (MGO) occurs in diabetes. MicroRNA-204 is an important intracellular marker in the diagnosis of endoplasmic reticulum stress. Crocin (Crn) has beneficial effects for diabetes, but the effect of Crn on MGO-induced diabetic nephropathy has not been investigated. The current research evaluated the effects of Crn and metformin (MET) on diabetic nephropathy induced by MGO in male mice.Materials and Methods: In this experimental study, 70 male NMRI mice were randomly divided into 7 groups: control, MGO (600 mg/Kg/d), MGO+Crn (15, 30, and 60 mg/kg/d), MGO+MET (150 mg/kg/d), and Crn60 (60 mg/kg/d). Methylglyoxal was gavaged for four weeks. After proving hyperglycemia, Cr and MET were administered orally in the last two weeks. Biochemical and antioxidant evaluations, microRNA expression, and histological evaluation were assessed.Results: The fasting blood glucose, urine albumin, blood urea nitrogen, plasma creatinine, malondialdehyde, Nrf2, miR-204, and miR-192 expression increased in the MGO group. These variables decreased in Crn-treated animals. The decreased levels of superoxide dismutase, catalase, glyoxalase 1, Glutathione, and miR-29a expression in the MGO group improved in the diabetic-treated mice. Histological alterations such as red blood cell accumulation, inflammation, glomerulus diameter changes, and proximal cell damage were also observed.Conclusion: Our study indicated that Crn and MET attenuated renal damage by inhibiting endoplasmic reticulum stress.

Abstract Background Diabetic nephropathy (DN) is one of the most important complications of type 2 diabetes (T2DM). Oxidative stress and inflammatory cytokines play an essential role in the development and progression of DN. Despite adopting appropriate therapies, many patients with DN progress to end-stage renal disease (ESRD). Therefore, exploring innovative strategies for better management of DN is crucial. Crocin, a natural compound found in saffron, has profound antioxidant, antifibrotic and anti-inflammatory properties. This study aimed to evaluate the therapeutic effects of crocin in attenuation of the progression of DN. Methods In this randomized, triple-blind, placebo-controlled clinical trial, 44 patients with T2DM and microalbuminuria were randomly assigned to receive either crocin (15 mg/day) or a placebo for 90 days. Eventually, 40 patients completed the study: 21 patients in the crocin group and 19 in the placebo group. The primary outcome was a change in urine Albumin-to-Creatinine Ratio (uACR) from baseline to the end of the treatment period. We also evaluated metabolic, anthropometric, and biochemical parameters as the secondary outcomes. Results The results of the present study showed that uACR increased in both groups, but the increment was not significantly higher in the crocin group compared with the placebo. Serum levels of transforming growth factor-β (TGF-β) decreased in the crocin group and increased in the placebo group, but none of these changes was significant. Crocin significantly reduced triglyceride (TG) as an important metabolic parameter (P-Value = 0.03). Conclusion This study has shown that crocin may be a safe and potential adjunct to conventional therapies for DN patients but because of our limitations such as short duration of the treatment period, and prescribing low doses of crocin, we could not achieve the significant level.

Abstract Background Psoriasis is a chronic inflammatory disorder of the skin; the hallmark of psoriasis is sustained inflammation that leads to uncontrolled keratinocyte proliferation and dysfunctional differentiation. Psoriasis shows clear autoimmune-related pathomechanisms, in which autoantigen-specific T cells contribute to the development, chronification, and overall course of the disease. Psoriasis is primarily a skin disease, but other internal organs may be involved; affliction of the joints is well established, but kidney involvement is yet to be universally agreed upon, although some recent studies have linked psoriasis to kidney disease and certain glomerular diseases including secondary renal amyloidosis, Ig A nephropathy, and membranous glomerulopathy. Case presentation and conclusion In this paper, we report a case of primary membranoproliferative glomerulonephritis (MPGN) with nephrotic impure syndrome in a psoriatic patient. The etiological investigation was negative with normal serum complement and ASO titers and were negative for HBV, HCV, HIV, and ANA. The patient improved on prednisolone and angiotensin-converting enzyme inhibitors. To our best of knowledge, cases of MPGN associated with psoriasis are rare and we would like to shed light on this association.

Several risk prediction models of Contrast-associated acute kidney injury (CA-AKI) in patients undergoing cardiac angiography or angioplasty are available. However, the lack of extensive external validations limits generalizability and clinical acceptance. This study conducted the external validation of three CA-AKI predictive risk models (Chen’s, Inohara’s, and Tziakas’ risk models) and determined the incidence of CA-AKI in Thai patients undergoing cardiac angiography or angioplasty. A total of 647 medical records of patients who underwent elective cardiac angiography (n=446) and angioplasty (n=201) were reviewed. Fifty-five percent were male, mean age 62.6±10.2 years, and mean estimated glomerular filtration rate (eGFR) 69.93±24.30 ml/min/1.73 m2). Incidents of CA-AKI, defined as an absolute increase of serum creatinine of at least 0.3 mg/dL within 48 hours or a relative increase of at least 50% within seven days after the procedure, were collected. The results showed that 78 patients (12.1%) had developed CA-AKI. Chen’s, Inohara’s, and Tziakas’ predictive risk models exhibited low discriminative ability with c-statistic of 0.571, 0.551, and 0.530, respectively. Due to low discriminative capability, these risk models may have low sensitivity to predict CA-AKI in Thai patients undergoing elective cardiac angiography or angioplasty.

Background: Polyomavirus, known as BK virus, is an important cause of allograft dysfunction in renal transplant patients, leading to BK virus nephropathy. The main study objectives were to assess the disease incidence and disease course in pediatric patients, and assess the diagnostic accuracy of BK screening for asymptomatic patients. Methods: This is a single‐center observational study, which included 81 pediatric renal allograft recipients that were transplanted and/or followed at King Fahad Specialist Hospital‐Dammam, Saudi Arabia. Screening for BK virus was performed prospectively according to a predetermined hospital protocol. Our BK screening protocol consisted of periodic quantitative real time polymerase chain reaction test in the plasma. In patients with deranged graft function, graft biopsies were evaluated for the presence of BK nephropathy. Results: Our study detected BK viremia in 14 patients (17.3%), while BK nephropathy occurred in seven patients (8.6%). The onset of BK viremia had bimodal distribution, 78 percent occurring within first year post‐transplantation, while 21.4% occurred late. Patients who developed BK nephropathy had a higher BK level than BK viremia patients, for both mean and peak values (p =.02, p =.02). A BK cutoff level of 40 000 copies/mL showed sensitivity and specificity of 85.7%, 85.7%, respectively, in predicting the conversion of BK viremia to BK nephropathy. Conclusions: BK viremia and BK nephropathy occur in pediatric patients with similar incidence rates compared to adult patients. Protocolized screening led to early detection of viremia, and could predict the conversion of BK viremia to BK nephropathy and allow for early immunosuppression modulation. [ABSTRACT FROM AUTHOR]

Introduction. Albuminuria greater than 300mg/dL/24h (A1-300mg/g) is a characteristic of diabetic nephropathy (DN), which can trigger the development of advanced chronic kidney disease (ACKD). Objective. Identify genes regulated by miRNAs that are associated with DN through an in-silico analysis. Material and methods. Through the use of microarrays and bioinformatic analysis, potential miRNA target genes were identified: hsa-miR-126-3p, miR-320a-3p, and miR-1288-3p. These genes were subjected to signaling pathway analysis to identify processes associated with DN pathogenesis. Results. 57 target genes were identified from the analyzed miRNAs, which were associated with 14 genetic ontologies and 7 KEGG signaling pathways. These results allowed the generation of an in-silico model showing an interaction network between target genes regulated by miRNAs whose alteration can lead to the development of ND. Conclusions. In the in-silico model, the network of interactions found between target genes regulated by miRNAs could contribute to the understanding of the DN mechanism, opening the panorama for new research on genes and miRNAs that could be evaluated as markers in the early detection of DN. [ABSTRACT FROM AUTHOR]

The focal segmental glomerulosclerosis (FSGS) is one of the most frequent glomerulopathy in the world, being considered a significative public health problem worldwide. The disease is characterized by glomerular loss mainly due to inflammation process and collagen fibers deposition. STAT-3 is a transcription factor associated with cell differentiation, migration and proliferation and in renal cells it has been related with fibrosis, acting on the progression of the lesion. Considering this perspective, the present study evaluated the involvement of STAT-3 molecule in an experimental model of FSGS induced by Doxorubicin (DOX). DOX mimics primary FSGS by causing both glomerular and tubular lesions and the inhibition of the STAT3 pathway leads to a decrease in fibrosis and attenuation of kidney damage. We described here a novel FSGS experimental model in a strain of genetically heterogeneous mice which resembles the reality of FSGS patients. DOX-injected mice presented elevated indices of albuminuria and glycosuria, that were significantly reduced in animals treated with a STAT-3 inhibitor (STATTIC), in addition with a decrease of some inflammatory molecules. Moreover, we detected that SOCS-3 (a regulator of STAT family) was up-regulated only in STATTIC-treated mice. Finally, histopathological analyzes showed that DOX-treated group had a significant increase in a tubulointerstitial fibrosis and tubular necrosis, which were not identified in both control and STATTIC groups. Thus, our results indicate that STAT-3 pathway possess an important role in experimental FSGS induced by DOX and may be an important molecule to be further investigated. [ABSTRACT FROM AUTHOR]

Background: Elevated serum levels of osteopontin (OPN) have been associated with cardiovascular disease, diabetic nephropathy, and autoimmune disease activity. The aim of this study was to investigate the relationship between OPN serum levels and renal damage in type 2 diabetes patients. Methods: This analytical cross-sectional study was carried out in Yazd, Iran from April to September 2017. Micro-albuminuria and creatinine (Cr) in 750 patients were measured and 180 included patients were divided into the three groups of 60 subjects based on the level of micro-albuminuria; normal (group A), micro proteinuria (group B) and macro proteinuria (group C). Body weight, height, blood pressure, body mass index (BMI), HbA1c and OPN were assessed. Results: Among 179 patients, 60 of them were normal for proteinuria, 59 patients had micro-proteinuria and 60 ones had macro-proteinuria. The mean age of participants was 58.96 (±11.10) years (range 26-80 years), 90 patients (50.8%) were males and 88 ones (49.2%) were females. The mean OPN levels were significantly higher in group C compared to group B, and in group B compared to group A (P=0.0001). Serum OPN was correlated positively with HbA1c (P: 0.012), Cr (P=0.010) and glomerular filtration rate (GFR) (P=0.002). There was a significant difference in the mean of OPN level among the subgroups with the history of ischemic heart disease (IHD) and HbA1C (P=0.035, and 0.047 respectively). Conclusion: These findings suggest that OPN is involved in chronic disease activity, and there is an independent association between plasma levels of OPN, and nephropathy in diabetic patients. [ABSTRACT FROM AUTHOR]

Background: Type 2 diabetes mellitus (T2DM) is a chronic, metabolic disorder in which concomitant insulin resistance and b-cell impairment lead to hyperglycemia, influenced by genetic and environmental factors. T2DM is associated with long-term complications that have contributed to the burden of morbidity and mortality worldwide. The objective of this manuscript is to conduct an Exome-Wide Association Study (EWAS) on T2DM Emirati individuals to improve our understanding on diabetes-related complications to improve early diagnostic methods and treatment strategies. Methods: This cross-sectional study recruited 310 Emirati participants that were stratified according to their medically diagnosed diabetes-related complications: diabetic retinopathy, diabetic neuropathy, diabetic nephropathy, and cardiovascular complications. The Illumina's Infinium Exome-24 array was used and 39,840 SNPs remained for analysis after quality control. Findings: The analysis revealed the associations of various genes with each complication category: 1) diabetic retinopathy was associated to SHANK3 gene in locus 22q13.33 (SNP rs9616915; p=5.18 x10-4), ZSCAN5A gene in locus 19q13.43 (SNP rs7252603; p=7.55 x10-4), and DCP1B gene in locus 12p13.33 (SNPs rs715146, rs1044950, rs113147414, rs34730825; p=7.62 x10-4); 2) diabetic neuropathy was associated to ADH4 gene in locus 4q23 (SNP rs4148883; p=1.23 x10-4), SLC11A1 gene in locus 2q35 (SNP rs17235409; p=1.85 x10-4), and MATN4 gene in locus 20q13.12 (SNP rs2072788; p=2.68 x10-4); 3) diabetic nephropathy was associated to PPP1R3A gene in locus 7q31.1 (SNP rs1799999; p=1.91 x10-4), ZNF136 gene in locus 19p13.2 (SNP rs140861589; p=2.80 x10-4), and HSPA12B gene in locus 20p13 (SNP rs6076550; p=2.86 x10-4); and 4) cardiovascular complications was associated to PCNT gene in locus 21q22.3 (SNPs rs7279204, rs6518289, rs2839227, rs2839223; p=2.18 x10-4,3.04 x10-4,4.51 x10-4,5.22 x10-4 respectively), SEPT14 gene in locus 7p11.2 (SNP rs146350220; p=2.77 x10-4), and WDR73 gene in locus 15q25.2 (SNP rs72750868; p=4.47 x10-4). Interpretation: We have identified susceptibility loci associated with each category of T2DM-related complications in the Emirati population. Given that only 16% of the markers from the Illumina's Infinium Exome chip passed quality control assessment, this demonstrates that multiple variants were, either, monomorphic in the Arab population or were not genotyped due to the use of a Euro-centric EWAS array that limits the possibility of including targeted ethnicspecific SNPs. Our results suggest the alarming possibility that lack of representation in reference panels could inhibit discovery of functionally important loci associated to T2DM complications. Further effort must be conducted to improve the representation of diverse populations in genotyping and sequencing studies. [ABSTRACT FROM AUTHOR]

Introduction: Medical renal diseases stand as one of the major health problems in pediatric age group considering its morbidity/mortality and the subsequent management plans. Objectives: In this manuscript, the spectrum of histopathological patterns of medical nephropathic lesions in Egyptian pediatric patients over duration of five years is reported with clinical indications. Patients and Methods: We conducted a retrospective study for analysis of our pathological reports of renal needle biopsies during the period from January 2014 until January 2019. One hundred and sixteen cases were included. Results: The most commonly encountered pediatric renal pathology was minimal change disease (27.59%), followed by congenital glomerular diseases (22.41%), focal segmental glomerulosclerosis (12.93%), and thrombotic microangiopathy (7.76%). The most common clinical indication for biopsy was nephrotic syndrome (37.07%) followed by impaired renal functions with elevated serum creatinine (21.55%). In addition, we report very rare histological findings in few cases including infantile nephropathic cystinosis, Barakat syndrome and C3 glomerulopathy. Conclusion: Minimal change disease and congenital glomerular diseases accounted for half of pediatric renal pathologies in the study population. The most common clinical indication for renal biopsy was nephrotic syndrome. Electron microscopic examination and genetic studies are mandatory for proper evaluation of pediatric nephropathies. [ABSTRACT FROM AUTHOR]

Purpose: The high incidence of upper urinary tract urothelial carcinoma (UTUC) in Taiwan is largely due to exposure to aristolochic acid (AA), a principal component of Aristolochia-based herbal medicines. Here we systematically review the molecular epidemiology, clinical presentation and biomarkers associated with AA-induced UTUC. Methods: This is a narrative review. Medline, Embase, and Web of Science were searched from inception to December 31, 2021. Studies evaluating the association, detection, and clinical characteristics of AA and UTUC were included. Results: A nationwide database revealed 39% of the Taiwanese population had been exposed to AA-containing herbs between 1997 and 2003. Epidemiological reports revealed AA posed a significantly higher hazard for renal failure and UTUC in herbalists and the general population who ingested AA-containing herbs. The presence of aristolactam-DNA adducts and a distinctive signature mutation, A:T to T:A transversions, located predominantly on the non-transcribed DNA strand, with a strong preference for deoxyadenosine in a consensus sequence (CAG), was observed in many UTUC patients. Clinically, AA-related UTUC patients were characterized by a younger age, female gender, impaired renal function and recurrence of contralateral UTUC. To date, there are no preventive measures, except prophylactic nephrectomy, for subjects at risk of AA nephropathy or AA-related UTUC. Conclusion: AA exposure via Aristolochia-based herbal medicines is a problem throughout Taiwan, resulting in a high incidence of UTUC. Aristolactam-DNA adducts and a distinctive signature mutation, A:T to T:A transversions, can be used as biomarkers to identify AA-related UTUC. AA-related UTUC is associated with a high recurrence rate of contralateral UTUC. [ABSTRACT FROM AUTHOR]

Type 2 Diabetes Mellitus (T2DM) and cardiac hypertrophy (CH) are among the top ten leading cause of deaths, worldwide. T2DM and cardiac hypertrophy are the chronic diseases, have close association and direct life-threatening complications like stroke, myocardial infarction, retinopathy, nephropathy, and limb amputation. In addition to other medical approaches, miRNAs-based strategy is considered most efficient for early detection of chronic diseases and also has potential for the treatment of T2DM and cardiac hypertrophy like it is being used for cancer in clinical trials. MicroRNAs (miRNAs) are single stranded (non-coding) of 20 to 22 nucleotides sequences which bind to their target mRNA upon the complimentary basis, to silence the protein expression at post transcriptional level. Bioinformatic databases are used like online mendelian inheritance in man (OMIM), gene testing registry (GTR), TargetScan and ShinyGO for validation of disease linked genes and sorting the common miRNAs in both diseases, such as miR-30-5p/101-3p.2/190-5p/506-3p/9-5p/128-3p/137/96-5p/7-5p/107/101-3p.1/98-5p/124-3p.2/124-3p.116-5p/15-5p/497-5p/ 424-5p/195-5p/1271-5p, let-7-5p. Aforementioned databases were also used for the miRNAs which have more than one disease linked genes target in each pathological condition. Such miRNAs for cardiac hypertrophy are: miR-19-3p/183-5p.2/153-3p/372-3p/302-3p/520-3p/373-3p/129-5p/144-3p/139-5p and for T2DM are: miR-27-3p/206/1-3p/181-5p. This finding would be helpful for the appropriate selection of miRNAs and to design applicable research project in future. It will require more validation by using the miRNAs expression analysis, mimic, and anti-miRNA approach to check their potential against cardiac hypertrophy and T2DM. [ABSTRACT FROM AUTHOR]

Diabetes is the commonest cause of end‐stage kidney disease in many parts of the world, and many people on dialysis programmes live with diabetes. Such people are vulnerable to complications from their diabetes, and their care may be fragmented due to the many specialists involved. This updated guidance from the Joint British Diabetes Societies aims to review and update the 2016 guidance, with particular emphasis on glycaemic monitoring in the light of recent advances in this area. In addition, the guidance covers clinical issues related to the management of diabetes in people on peritoneal dialysis, along with acute complications such as hypoglycaemia and ketoacidosis, and chronic complications such as foot and eye disease. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the effect of fluorescein dye usage on renal function in patients with diabetic retinopathy (DR) and chronic kidney disease (CKD). Methods: Diabetic patients with retinopathy who were candidate for fundus fluorescein angiography (FA) were evaluated for serum creatinine and urea levels within five days prior to performing the FA. Serum creatinine levels of 1.5 mg/dl or more in males and 1.4 mg/dl or more in females were both identified as CKD and were included in the study. An increase of 0.5 mg/dl or 25% in creatinine after FA was considered as contrast-induced acute kidney injury (AKI). Estimated glomerular filtration rate (eGFR) was also calculated for all patients using a CKD-Epi formula. CKD grading was determined based on eGFR values. Results: Forty-two patients agreed to participate, of which 23 (54.8%) were male. Seventeen patients were identified with grade 3a or lower CKD, 12 with grade 3b, 11 with grade 4, and two with grade 5 CKD. Considering all grades of CKD, the mean blood urea before and after angiography was 58.48 ± 26.7 and 57 ± 27.81 mg/dl, respectively (P = 0.475). The mean serum creatinine before and after the test was 1.89 ±1.04 and 1.87±0.99 mg/dl, respectively (P = 0.993). The mean eGFR before and after the test was 44.024 ±23.5447 and 43.850 ±21.8581 mL/min/1.73 m2 (P = 0.875). Conclusion: According to the findings of this study, FA does not seem to further deteriorate kidney function in patients with diabetic associated CKD. [ABSTRACT FROM AUTHOR]

Diabetic retinopathy, neuropathy, and nephropathy occur in more than 50% of people with diabetes, contributing substantially to morbidity and mortality. Patient understanding of these microvascular complications is essential to ensure early recognition and treatment of these sequalae as well as associated symptoms, yet little is known about patient knowledge of microvascular sequalae. In this comprehensive literature review, we provide an overview of existing knowledge regarding patient knowledge of diabetes, retinopathy, neuropathy, and nephropathy. We also discuss health care provider's knowledge of these sequalae given that patients and providers must work together to achieve optimal care. We evaluated 281 articles on patient and provider knowledge of diabetic retinopathy, neuropathy, and nephropathy as well as predictors of improved knowledge and screening practices. Results demonstrated that patient and provider knowledge of microvascular sequalae varied widely between studies, which may reflect sociocultural or methodologic differences. Knowledge assessment instruments varied between studies with limited validation data and few studies controlled for confounding. Generally, improved patient knowledge was associated with greater formal education, longer diabetes duration, and higher socioeconomic status. Fewer studies examined provider knowledge of sequalae, yet these studies identified multiple misconceptions regarding appropriate screening practices for microvascular complications and the need to screen patients who are asymptomatic. Further investigations are needed that use well validated measures, control for confounding, and include diverse populations. Such studies will allow identification of patients and providers who would benefit from interventions to improve knowledge of microvascular complications and, ultimately, improve patient outcomes. [ABSTRACT FROM AUTHOR]

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