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To check adherence to the antihypertensive medication in patients with arterial hypertension and a possible impact of fixed-dose drug combinations, cardiovascular event in history, and diabetes on it. In this cross-sectional study, every fifth patient with arterial hypertension in two family medicine practices in Zagreb, Croatia (found by Medicus search engine) was analyzed during February 2022. We included medical records of 210 patients (116 males, 94 females) from which we checked the number and type of used antihypertensive medication (single pill or fixed- dose drug combinations), statin use, diabetes type 2 or cardiovascular event in history, and the date of the last lab test results. The patient was considered adherent if she/he regularly ordered hers/his prescribed medication from January to December 2021. Chi-square and Student t-test were used for statistical analysis in Statistica 12. There were no differences between genders. Women were slightly more adherent to the prescribed therapy than men (72.34 vs. 68.11%, P = 0.5076). Statins were prescribed in 65 (30.95%), fixed-dose combination in 139 (66.19%), 39 had diabetes (18.57%), and 28 patients had cardiovascular events in their medical history (13.33%). The adherence was not dependent on the patient’s age (66.75 vs. 66.64 years in adherent patients, P = 0.9509), the existence of diabetes (Chi2 = 1.093, 2, P = 0.2958) or previous cardiovascular event in medical history (Chi2 = 0.384, 2, P = 0.5351). Adherence correlated with the number of prescribed antihypertensive medications (r = 0.263 ; P < 0.05 ; and average 2.56 in adherent vs. 1.97 medication per day in non-adherent group, P < 0.001), especially if the therapy was in fixed-dose combination (Chi2 = 11.60, 2, P < 0.001). The age of the lab test results was less in adherent patients (1.25 vs. 1.86 years, P = 0.108). 116 patients (55.24%) had them in 2021, while 16 did not have any result in five and more years (7.14%). The adherence to antihypertensive therapy was similar between genders and correlated with the number of prescribed medications with significantly better results in patients with fixed-dose combinations. The existence of the previous cardiovascular event and type 2 diabetes did not show any benefit on this type of adherence.

The aim of this study was to determine the frequency of newly verified or worsened existing hypertension in patients who had COVID-19. In this case-control study which lasted from May 2021 to December 2021, 108 patients (49 males, 59 females) who have had COVID-19 were analyzed at the Emergency department in Clinical Hospital Merkur, a tertiary care center in Zagreb, Croatia. In order to be categorized as a COVID patient, a positive PCR test at a single point in time was required. According to the accepted definitions of COVID-19 and its manifestations in respect to time from a positive PCR test, the patients were divided into two groups: acute COVID patients (PCR test positive < 30 days ago) and post- acute COVID patients (PCR test positive > 30 days ago). Additionally, the post-acute group was subdivided into the following groups: sub-acute (30– 90 days from positive PCR test), chronic (90–180 days from positive PCR test), and “long COVID” (>180 days from positive PCR test). Patients’ age, history, BMI, laboratory values, and antihypertensive therapy were recorded. Out of 108 patients studied, 13 (12.04 %) had either newly verified (8) or worsened existing (5) arterial hypertension. Among those, the median time from a verified SARS-CoV-2 infection to onset of symptoms was 90 days. When divided into groups, 5 were in the acute, 3 in the sub-acute, 4 in the chronic, and 1 in the “long COVID” group. Compared to the rest of the study population, patients presenting with arterial hypertension had significantly higher systolic (median 155 vs. 126 mmHg, p = 0.004) and diastolic (median 90 vs 80 mmHg, p = 0.02) blood pressure and were non-significantly younger (median 48 vs 58 years, p = 0.067). Arterial hypertension following COVID-19, either newly verified or worsened existing, is a relatively common (12.04% of our patient pool) occurrence and more effort should be directed into evaluating patients’ blood pressure values following COVID-19 in order to make a timely diagnosis and start proper treatment early.

The aim of this study was to determine if patients with the hypertensive crisis have higher pulse wave velocity compared to the patients with arterial hypertension without it. In this case- control study which lasted from January 2020 to December 2021, 61 patients (36 males, 25 females) with the hypertensive crisis were analyzed at the Emergency department in Clinical Hospital Merkur, Zagreb. The hypertensive crisis was defined as a rapid increase in systolic blood pressure above 180 and/or diastolic above 120mmHg (SBP range 181– 208mmHg). On the other hand, in the control group, we analyzed 45 patients (24 males, 21 females) with confirmed arterial hypertension by a 24h- ambulatory blood pressure monitor (BTL Cardiopoint, SBP > 130/80mmHg or taking antihypertensives) without evidence of hypertensive crisis (SBP range 115–156mmHg) in two family medicine practices. Elementary lab results and pulse wave velocity (by Agedio B900) were checked in all patients. Patients were divided into two additional groups by age (51–60, 42 patients and 61–70 years, 64 patients). Mann- Whitney U test was used for the analysis of non- parametric variables in Statistica v.10.0. Patients with hypertensive crisis had a significantly higher heart rate (median 78 vs. 69 bpm, U = 714 ; p < 0.001), fasting glucose (median 5.5 vs. 6.0 mmol/L, U = 804.5 ; p < 0.01), body mass index (median 31.0 vs. 27.9 kg/m2, U = 889 ; p < 0.001), nocturnal SBP drop (median 15.5 vs. 9.8%, U = 386 ; p < 0.05), and augmentation index (median 42 vs. 19%, U = 686 ; p < 0.001). In both younger and older group, patients with hypertensive crisis had statistically significantly higher pulse wave velocity (median younger: 9.3 vs. 8.1m/s, U = 65.5 ; p < 0.001 ; older: 10.7 vs. 9.0m/s, U = 19 ; p < 0.001) shown in the Figure 1. In younger group patients with hypertensive crisis have 8.5 times higher chances of having pulse wave velocity above reference value (>8.0m/s ; CI = 1.57–46.87, p < 0.001) while in older group that chance was 108 times higher than in controls (reference value >9.5m/s ; CI = 13.83–843.33, p < 0.001). Patients with hypertensive crisis had statistically higher pulse wave velocity values, heart rate, fasting glucose, body mass index, and nocturnal SBP drop compared to patients with arterial hypertension without crisis.

Objective: The aim of this study was to determine risk factors for hypertensive crisis development just as an impact of the kidney function on it. Design and method: From January to October 2019, 237 patients (109 males, 128 females) with hypertensive crisis were analyzed at the Emergency department in Clinical Hospital Merkur, Zagreb. We defi ned the hypertensive crisis as a rapid increase in blood pressure above 180/120mmHg (SBP range 182-260mmHg). Hypertensive crises were divided into two subgroups due to the evidence of endorgan damage. Elementary lab results and pulse wave velocity were checked in all patients. Results: Hypertensive urgency was found in 184 patients (77.64%), emergency in 53 (22.36%). Comparison of these two subgroups showed that patients with an emergency were signifi cantly older (70.51 vs. 64.44 years, p

We present a case of a 50-year-old man with advanced liver cirrhosis and native valve infective endocarditis caused by methicillin- resistant Staphylococcus epidermidis. Bacterial infections are one of the most common complications of liver cirrhosis, but reports of infective endocarditis in patients with liver cirrhosis are relatively rare. Because of vulnerability of patients with advanced cirrhosis for developing infections, it is necessary to pay attention to the pathogens that are sometimes considered contamination and actively seek for the seat of infection, even in less expected areas (e.g., native heart valves without a history of heart disease).

Renal sympathetic denervation (RSD) could be an effective antihypertensive treatment of resistant hypertension that triggers additional positive effects on glucose metabolism and insulin sensitivity in type 2 diabetes mellitus. We report the effects of RSD in a patient with chronic kidney disease, type 2 diabetes mellitus and resistant hypertension, manifesting as blood pressure reduction with dipping pattern restoration, followed by nephrotic proteinuria alleviation. The non-dipping blood pressure pattern and proteinuria increase the risk of cardiovascular complications and accelerate kidney disease progression. Thus, further research documenting the frequency and investigating the mechanisms of these effects reported after RSD in chronic kidney disease patients with type 2 diabetes mellitus and resistant hypertension is necessary for the benefit of this high-risk patient population.

Subacute granulomatous thyroiditis is an inflammatory thyroid condition that is presumed to be caused by a viral infection or postviral inflammatory process. It is characterized by neck pain, usually a tender diffuse goiter, and thyrotoxicosis. A case is presented of subacute granulomatous thyroiditis in an adult woman who had no neck pain but presented with morning stiffness in the small joints of the right hand, intermittent abdominal pain, malaise, fever, and myalgia. After the diagnosis had been established, she was treated with propranolol and acetylsalicylic acid, and has fully recovered. In conclusion, this disease may be difficult to diagnose, especially if there is a combination of fever and increased aminotransferases, which can lead to a wrong diagnostic approach.

In patients with resistant hypertension (RH) we investigated the importance of urinary neutrophil gelatinase-associated lipocalin (uNGAL- a chemiluminescent microparticle immunoassay (CMIA) method became using (Abbott Diagnostics) for the measurement of NGAL in urine samples) and incidence of chronic kidney disease using the Modification of Diet in Renal Disease Study (MDRD) and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations in estimating glomerular filtration rate (eGFR) based on standardised serum creatinine method traceable to isotope dilution mass spectrometry (IDMS) method. It would have been difficult to predict that levels of these biomarker would perform better organ damage than traditional measurements of kidney function such as standardised serum creatinine, MDRD, or CKD-EPI equations in special population such as RH. Serum creatinine concentrations were measured in 50 patients (24M:26F from RH Registar in Clinical Hospital Merkur) by the kinetic Jaffe method. There were no significant differences between the GFR values derived by MDRD and CKD-EPI equations in the group of patients with RH. 62% of patients have eGFR60 mL/minl/1.73 m2, while a 38% of patients have eGFR60 mL/min/1.73 m2. The measurement of NGAL in urine samples of 40 patients with RH showed no difference and seems to be of no use in further determination of renal impairement. Higher value of uNGAL in some resistant hypertension patients could have link in the repair stage after AKI and would reveal pathways that could link AKI and CKD.

Changes in renal microcirculation represent the important factor in the progression of cardiovascular and renal complications. Microalbuminuria is the earliest indication that indicates the kidney and systemic microcirculatory disorder. The importance of microalbuminuria as a risk factor of increased cardiovascular mortality is well documented. It is therefore extremely important to explore all factors that can prevent the development of microalbuminuria including glomerular hyperfiltration. Is it possible to reduce glomerular hyperfiltration and slow progression of diabetic nephropathy?

To evaluate efficacy and safety of CERA (continuous erythropoietin receptor activator) administration for correcting anemia in the patients with chronic kidney disease (CKD), not on dialysis.We performed observational study on 27 CKD patients in stage 4 or 5 with renal anemia requiring use of erythropoiesis-stimulating agents (ESA). All patients received CERA (Mircera; Roche, Basel, Switzerland) subcutaneously in dose of 0.6 microg per kg every two weeks during the correction phase of anemia treatment or once monthly during the maintenance treatment. Dose of CERA was modified according to manufacturer instructions. Iron supplementation was administrated orally or intravenously in order to achieve serum ferritin 200-500 microg/L. Patients were followed up to 1 year (from 3-12 months). Response criteria for CERA were Hb increase10 g/L above baseline or Hbor = 110 g/L.Hb statistically significant (p0.05), increased during the observation period. The median at baseline was 94 g/L and after 6 months and one year were 108 g/L and 114.5 g/L respectively. Furthermore, the range of the lowest and highest values of Hb gradually decreased indicating less Hb fluctuation. After one year, all patients had Hb range 100 g/L to 120 g/L. There were no statistically significant differences between Hb between groups of patients stratified according to the primary kidney disease and age. During the study period two patients died due to myocardial infarction, probably not associated with CERA administration according to observed Hb levels (103 and 110 g/L). Only registered side effect was slight increase in arterial pressure, controlled with antihypertensive drugs. The majority of patients had reported better exercise tolerance and sleep and less irritability.The results of this observational study suggest that the use of CERA is effective and safe and leads to a successful correction of anemia in CKD patients who have not yet started renal replacement therapy.

Hyperfiltration has been documented in type 1 diabetes and may contribute to the high risk for development of albuminuria and progression of nephropathy. However, recent studies suggest that the risk of progression to albuminuria in type 1 diabetes was not increased by hyperfiltration. We investigated associations of estimated glomerular filtration rate (eGFR) and urinary albumin excretion rate (UAE) in normoalbuminuric type 1 diabetic patients. Study included 313 normoalbuminuric patients with type 1 diabetes, none showed signs of adrenal, renal, or cardiovascular diseases. GFR was estimated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula. Glomerular hyperfiltration was defined as eGFRor = 125 mL min(-1) 1.73 m(-2). Renal hyperfiltration was present in 12% of the study group. Subjects with eGFRor = 125 mL min(-1) 1.73 m(-2) were younger, had shorter duration of diabetes, lower levels of total and LDL cholesterol, and higher HbA1c than subjects with an eGFR below 125 mL min(-1) 1.73 m(-2). Type 1 diabetic patients with hyperfiltration also had significantly lower UAE. In a multiple logistic regression analysis, higher eGFR was associated with lower UAE. Our results indicate that normoalbuminuric type 1 diabetic patients with hyperfiltration have lower UAE than those with renal function in the normal range. Together with other recent studies this may suggest that creatinine-based estimates of GFR indicating hyperfiltration is not associated with higher UAE and subsequent development of microalbuminuria.

A 31-year-old woman suffering from diabetes type1 and terminal kidney disease, with simultaneously transplanted kidney and pancreas, developed an episode of acute organ rejection caused by antibodies. The management of organ rejection was complicated by cytomegalovirus viremia, with accompanying leukopenia and neutropenia. The patient also developed invasive aspergillosis of the lungs, which progressed and disseminated hematogenously to the thyroid gland and the skin. Due to resistance to classical antimycotic therapy, the patient was treated with a combination of caspofungin and variconazole. In the beginning of treatment, the effects of this combined therapy were not evident due to strong immunosuppression caused by antimycotic immunoglobulin, which the patient had been administered on her previous hospital stay to treat acute kidney transplant rejection caused by antibodies, as well as due to immunosuppression caused by tacrolimus, mycophenolate mofetil and prednisone. On combined therapy with antimycotic drugs and supportive therapy, the patient was completely cured.

Amyloidosis is a clinical entity that results from deposition of an extracellular protein material that causes disruption in normal architecture and impairs function of multiple organs and tissues. Secondary amyloidosis (AA) is a rare but serious complication that appears in the context of cancer, chronic inflammation, and chronic infectious disease, including rheumatoid arthritis. Renal failure is the most common clinical presentation of AA, ranging from nephrotic syndrome and impaired renal function to renal failure, with a potential for high morbidity. We present a case of a 52-year-old female patient diagnosed with rheumatoid arthritis at age 27. She was hospitalized due to worsening clinical condition. Physical examination revealed marked peripheral edema in both lower extremities. Laboratory tests showed an increase of inflammatory reactants, anemia, electrolyte disbalance, and severe hypoalbuminemia and hypoproteinemia. She had proteinuria 15.4 g/24 h and renal function estimated by creatinine clearance was 78 mL/min, within the second degree of chronic kidney disease. Renal biopsy was performed for evaluation of renal insufficiency with nephrotic range proteinuria. Congo red staining showed the presence of characteristic amyloid deposits that immunoreacted with the antibody against amyloid A protein, thus confirming the diagnosis of secondary amyloidosis.

Plastic bronchitis is a rare disorder characterized by formation and sometimes dramatic expectoration of bronchial casts. It may occur at any age, but most published cases refer to pediatric population. We report a case of an 81-year-old man hospitalized at intensive care unit, who presented with the appearance of plastic bronchitis type I. He had profuse expectoration of several pieces, a few cm long and up to 1 cm wide, of wormlike reddish-brownish "tissue". Histologically, it was a slimy purulent secretion with abundant fibrin and blood and with cytopathic effect of herpes virus. The pathogenesis of plastic bronchitis is not clear.

In December 2005, the 55-year-old patient was hospitalized because of acute kidney failure and suspected hemorrhagic fever. The physical examination showed splenomegaly (spleen ultrasound-18 cm in large diameter, and 11 cm by palpation) with thrombocytopenia and anemia. He underwent kidney biopsy which described infiltration of small B cell lymphocytes with positive lambda chains. His bone marrow showed infiltration of atypical lymphocytes, and flow cytometry was typical of B-cell CLL. Patient started therapy with corticosteroids (methylprednisolone 80 mg iv) and continued treatment with prednisone (Decortin 20 mg tablets) and chlorambucil (Leukeran 16 mg tablets) through three days. An addition to therapy lead to an increase in platelet count, creatinine level decline and recovery of renal function was observed. He was treated with 6 cycles of therapy with prednisone and chlorambucil and achieved a satisfactory therapeutic effect with adequate hematologic parameters and less severe splenomegaly. Maintenance therapy was continued with prednison at daily dose of 10 mg. Our patient is one of the amongst previously reported as an example of a rare complication of CLL'with leukemic infiltrate causing acute renal insufficiency. Renal biopsy is necessary to confirm the diagnosis. This complication appears to respond well to a variety of treatments. Our patient achieved complete resolution of renal failure and partial hematological response with combination of chlorambucil and prednisone.

Hyperhemolysis syndrome usually occurs in patients with sickle cell disease and possibly thalassemia who receive multiple transfusions. There are only few clinical reports on patients without hemoglobinopathies as in this report. Our patient was diagnosed with hyperhemolytic reaction and was infused with IVIG and methylprednisolone for several days. Signs of tissue hypoxia developed along with increased cardiac enzymes, hepatocellular and cerebrovascular injury, and finally death. On autopsy, there was no evidence for hemolytic uremic syndrome or thrombotic thrombocytopenic purpura.

Red blood cells (RBC) normally lose their nuclei before appearing in peripheral blood. After having undergone differentiation in bone marrow, blood cells must cross the blood-marrow barrier to enter the bloodstream. Erythroblasts, or nucleated red blood cells (NRBC), do not distort easily, so they cannot escape this barrier. Therefore, with the exception of the neonatal period, the presence of NRBCs in peripheral blood is always a pathologic finding. NRBCs may be found in the course of severe diseases and are associated with poor prognosis and higher mortality. The underlying pathophysiology of NRBCs in peripheral blood is not fully understood. It is hypothesized that their appearance could be provoked by either increased erythropoiesis or bone marrow micro-architectural damage mostly caused by inflammation and/or decreased tissue oxygenation. In addition, it is known that the mortality is higher in NRBC-positive patients as compared with NRBC-negative patients. Hereby we present a patient admitted to the hospital with the symptoms of cardiac failure and decompensated liver cirrhosis. The patient was already known to have liver cirrhosis of ethylic etiology, cardiac decompensation caused by hypertensive heart disease with permanent atrial fibrillation, chronic obstructive pulmonary disease, diabetes mellitus type 2, and cholelithiasis. During hospital stay, the patient developed acute pancreatitis and, soon after that, a stroke with left hemiparesis followed by cardiopulmonary arrest. Then he was transferred to the intensive care unit. Despite appropriate therapy, intensive care treatment and cardiopulmonary support, the patient's general state worsened, he developed multiple organ failure and died on day 10 of intensive care unit stay. Three days earlier, NRBCs were detected in peripheral blood and their concentration increased during the next two days before death. NRBCs are known to appear 1-3 weeks before death, but their appearance does not seem to be related to one particular cause of death. Still, detection of NRBCs is an independent risk of poor outcome, where the mortality increases with the increasing NRBC concentration. Detection of NRBCs in blood is a relatively early phenomenon prior to death, so screening for NRBCs may aid in the early identification of patients at high risk, and in making duly decision for NRBC-positive patients to obtain ongoing intensive care treatment.

The leading causes of death in patients with chronic kidney disease (CKD) are cardiovascular diseases, regardless of the stage of disease or method of renal replacement therapy. On the other hand, CKD is a major risk factor for cardiovascular complications after acute myocardial infarction, as well as for adverse outcome in patients with chronic heart failure. In the present study we prospectively followed-up nephrological interventions in cardiology wards in order to determine changes in indications, treatment possibilities and outcome of patients. All patients treated at cardiology ward of the Clinical Hospital Centre Zagreb and requiring renal replacement therapy from January 2003 to December 2009 were included in the investigation. Cardiology hospital unit (intensive care or regular hospital cardiology ward), age, gender, Sepsis-related Organ Failure Assessment (SOFA) score, indication for dialysis, primary diagnosis, vascular access, methods of treatment, number of treatments, prescribed and delivered dose of dialysis and outcome were recorded. Patients were followed up until death during hospitalization or discharge from the hospital. From January 2003 to December 2009, 251 patients had been hospitalized at different cardiology wards and required renal replacement therapy. Mean age was 64.95 years (range 22 to 97 years), and there were 27.8% female patients. 52.9% of patients were hospitalized in the coronary intensive care unit. SOFA score had increased during the observed period from average 6.5 in 2003 to 13.45 in 2009. Specific knowledge with close collaboration between nephrologists and cardiologists is needed to achieve optimal outcome in this complex condition.

Amyloidosis is a clinical entity that results from deposition of an extracellular protein material that causes disruption in normal architecture and impairs function of multiple organs and tissues. Secondary amyloidosis (AA) is a rare but serious complication that occurs in the context of cancer, chronic inflammation and chronic infectious diseases, including inflammatory bowel disease, mainly long-standing Crohn's disease. Renal failure is the most common clinical presentation of AA, ranging from nephrotic syndrome and impaired renal function to renal failure, with a potential for high morbidity. The incidence of the association of secondary amyloidosis in patients with Crohn's disease has been reported to be 0.5%-8%. We present a case of a 39-year-old male patient diagnosed with Crohn's disease at age 21 and submitted to right hemicolectomy because of ileus 17 years before. Thereafter, he was treated with corticosteroids for 15 years and with azathioprine for a short period; in the last three years he was on therapy with mesalazine alone. He was hospitalized due to worsening clinical condition and re-evaluation of the underlying disease. Physical examination revealed marked peripheral edema in both lower extremities. Endoscopic and radiographic examinations confirmed the underlying disease activity. Laboratory tests showed an increase of inflammatory reactants, anemia, hypocalcemia, and severe hypoalbuminemia and hypoproteinemia. He had proteinuria over 24 g/L and creatinine clearance of 66 mL/min, falling within second grade of chronic kidney disease. Renal biopsy was performed for evaluation of renal insufficiency with nephrotic range proteinuria. Congo red staining showed the presence of characteristic amyloid deposition; deposits immunoreacted with the antibody against amyloid A protein, confirming the diagnosis of secondary amyloidosis. The patient was suggested active induction treatment with corticosteroids and azathioprine to achieve remission of Crohn's disease, thereafter treatment with infliximab, but he did not consent with this therapy at that time. Studies with infliximab have demonstrated a decrease in SAA circulating levels and proteinuria, as well as stabilization of renal function. Amyloidosis is frequently described as a major cause of death in patients with Crohn's disease, with long-term mortality between 40% and 60%. Various therapeutic attempts such as azathioprine, colchicine, dimethyl sulfoxide, infliximab, and elemental diets have been tried but there is no definite treatment for secondary amyloidosis in Crohn's disease. Kidney transplantation may offer the best prospects for patients with Crohn's disease who develop amyloidosis and end-stage renal failure.

Lipoproteins may contribute to diabetic nephropathy. Although elevated total HDL cholesterol levels have been shown to protect from coronary artery disease and nephropathy in many studies, HDL can be subdivided into at least two major subclasses, which are thought to differ in the ability to protect against atherosclerosis. The objective of this study was to determine the relationship between serum lipids and HDL subclasses with albuminuria in patients with type 1 diabetes.We analyzed lipid profiles of 259 patients with type 1 diabetes and normal thyroid function. Patients were classified as normoalbuminuric (albumin excretion rate30 mg/24 h, n = 215) and microalbuminuric (albumin excretion rate 30-300 mg/24 h, n = 44) in at least two urine collections. None showed signs of adrenal, thyroid, renal or cardiovascular disease, or received drugs, apart from insulin, that could attenuate glucose metabolism, serum lipids or renal function. Total, LDL, HDL, HDL2, HDL3, VLDL cholesterol and triglycerides were measured by an enzymatic colorimetric method and urinary albumin concentration was determined by an immunoturbidimetric assay.Patients with microalbuminuria had higher levels of total cholesterol (5.07 vs. 5.02 mmol/L, Mann Whitney=6874, P = 0.666), LDL cholesterol (2.81 vs. 2.80 mmol/L, Mann Whitney = 6964, P = 0.778), VLDL cholesterol (0.57 vs. 0.48 mmol/L, Mann Whitney = 6268, P = 0.151) and triglycerides (1.27 vs. 1.08 mmol/L, Mann Whitney = 6283, P = 0.158), and lower levels of HDL cholesterol (1.68 vs. 1.73 mmol/L, Mann Whitney = 6501, P = 0.293) and HDL3 cholesterol (1.15 vs. 1.16 mmol/L, Mann Whitney = 6991, P = 0.812); however, these differences were not statistically significant. In contrast, HDL2 cholesterol levels were significantly lower in those who had microalbuminuria compared with those who had normoalbuminuria (0.50 vs. 0.57 mmol/L, Mann Whitney = 5600, P = 0.01).Microalbuminuria is the earliest clinical indicator of diabetic nephropathy. Clustering of coronary artery disease with nephropathy has been shown previously in patients with type 1 diabetes. Specific effects of HDL subclasses on cardiovascular disease have also been observed, i.e. a protective effect of large HDL subfractions (HDL2) and an increased risk for small HDL particles (HDL3). Results of the present study showed that lower levels of HDL2 cholesterol were associated with microalbuminuria in patients with type 1 diabetes. Whether higher HDL2 cholesterol levels may be protective against the development of microalbuminuria in patients with type 1 diabetes can only be determined in long-term studies.

Insulin resistance has been documented in type 1 diabetes and may contribute to the high risk for cardiovascular disease in this population and progression of nephropathy. We investigated associations of renal parameters, including urinary albumin excretion rate (UAE), serum creatinine and creatinine clearance, with surrogate measure of insulin sensitivity calculated using a formula derived from euglycemic-hyperinsulinemic clamp studies (estimated glucose disposal rate, eGDR). Study included 353 patients with type 1 diabetes, none showed signs of adrenal, thyroid, renal, or cardiovascular diseases. Insulin sensitivity was measured with eGDR calculated with the equation: 24.31-(12.22xWHR)-(3.29xHT)-(0.57xHbA1c). The units were mgkg(-1)min(-1); WHR=waist to hip ratio; HT=hypertension. Correlations and logistic regression analysis were performed to identify relationships between renal parameters and eGDR, individual components of insulin resistance and risk of insulin resistance. UAE and serum creatinine significantly correlated with insulin resistance measured by eGDR (r=-0.13, and -0.17, all p0.05), and its components disorders, WHR and HbA1c. After stratifying patients in quartiles of eGDR, those in the upper quartile of the eGDR had significantly reduced levels of UAE and serum creatinine, compared to subjects in lowest quartile. In a logistic regression analysis risk for development of insulin resistance in our subjects were independently predicted only by UAE (odds ratio = 1.01, p0.01). Our results provide evidence of associations between insulin resistance and its components disorders with renal parameters, such as UAE and serum creatinine. Insulin resistance, measured with eGDR, predicts the increment in UAE in subjects with type 1 diabetes. Since progression to microalbuminuria is likely to occur in majority of diabetic patients, there is a need to further explore the role of risk factors such as insulin resistance.

Alergijski intersticijski nefritis (AIN) uzrokovan lijekovima rijedak je oblik bubrežne bolesti koji se klinički primarno manifestira akutnom bubrežnom insuficijencijom. Najčešća etiopatogeneza AIN-a reakcija je preosjetljivosti na lijekove među kojima su najzastupljeniji antibiotici. Najvažnija dijagnostička metoda u bolesnika sa sumnjom na AIN jest biopsija bubrega. Uz ukidanje uzročnog lijeka, u liječenju AIN preporučuje se primjena glukokortikoida, u dozi od 1 mg/kg/dan s postepenim snižavanjem doze, u trajanju do 3 mjeseca. U ovom radu, prikazali smo 10 bolesnika kod kojih je nakon pregleda bubrežnog bioptata s nalazom AIN-a, retrospektivno učinjena analiza kliničkih i biokemijskih podataka. Definirane su četiri različite uzročne skupine lijekova AIN-a, a najčešći su bili antibiotici. U kliničkoj prezentaciji dominirala je akutna bubrežna insuficijencija s medijanom serumskog kreatinina od 497,5 µmol/L. Svi bolesnici osim jednoga liječeni su preporučenim dozama glukokortikoida. Troje bolesnika liječeno je i hemodijalizom. U svih bolesnika došlo je do oporavka bubrežne funkcije, uz medijan serumskog kreatinina nakon tromjesečnoga glukokortikoidnog liječenja (u sedmero bolesnika) od 152 µmol/L (p=0,018)., The allergic interstitial nephritis (AIN) is a rare renal disorder which is commonly clinically presented with an acute renal failure. AIN is the most frequent result of the hypersensitivity related to drugs (most often antibiotics). In the patients with clinical suspicion to a drug related AIN, kidney biopsy is the most important diagnostic procedure. Except of causative drug discontinuation, AIN therapy is based on high dose glucocorticoids 1 mg/kg/day with dose tapering during consecutive 3 months. In the present work, we have shown 10 patients with drug induced AIN. We identified 4 causative drug groups among which most frequent were antibiotics. In clinical presentation of our patients acute renal failure was dominant and median of baseline serum creatinine was 497.5 µmol/L. In all patients the kidney biopsy was performed and nine patients (90%) have been treated with recommended glucocorticoid regimen, additionally, in 3 patients hemodialysis was introduced. In all patients, reduction in serum creatinine value was achieved with serum creatinine median of 152 µmol/L after a three-month glucocorticoid treatment (p=0.018).

We present a patient who was referred to the emergency services because she took an unknown quantity of ketoprofen tablets. After approximately 24 hours the patient presents with an acute ishemic stroke, myocardial infarction, and worsning renal fenction. In our patient, unforunately, we not measured concentration of ketoprofen, but given the severity of the clinical picture, we belive that the ketoprofen could certainly contribute to its occurrence.

The primary glomerular disease in patients with diabetes mellitus is rare. Several reports have shown that primary glomerular diseases can be superimposed on diabetic nephropathy. The recognition of nondiabetic glomerular diseases in diabetic patients is of utmost importance since they might be successfully treated. This would positively affect the otherwise poor prognosis of renal disease in diabetic patients. The suspicion on nondiabetic renal disease is raised by the appearance of urinary abnormalities such as hematuria, massive nephrotic proteinuria or deterioration in renal function in patients with diabetes mellitus but without coexisting diabetic retinopathy. We report on diabetic patients who underwent renal biopsy because of the massive nephrotic proteinuria and non-nephrotic proteinuria without diabetic retinopathy, hematuria, and because of the deterioration of renal function. On pathohistological examination different types of primary glomerular diseases were found. The diagnosis and the treatement of glomerular diseases improved the renal prognosis in some of these patients.

U bolesnika s reumatoidnim artritisom (RA) često je zahvaćen bubreg. Klinički se bubrežna bolest očituje proteinurijom (često nefrotskog ranga) i mikrohematurijom uz razvoj bubrežne insuficijencije. Bubrežnu bolest u bolesnika s RA nazivamo reumatoidnom nefropatijom a posljedica je imunološke upale u glomerulu i nefrotoksičnog učinka lijekova koji se uobičajeno primjenjuju u liječenju RA (NSAR i DMARD). Najčešće u bolesnika s RA patohistološki u tkivu bubrega nalazimo amiloidozu, potom glomerulonefritis i intersticijski nefritis. U radu prikazujemo 15 bolesnika, od toga 10 žena i 5 muškaraca prosječne dobi 60,2 godine, s prosječnim trajanjem RA od 19,4 godine i razvijenim znakovima reumatoidne nefropatije. Svim bolesnicima učinjena je biopsija bubrega, te je u petero bolesnika patohistološki utvrđena amiloidoza, u troje IgA nefropatija i FSGS, dok je mezangio-proliferativni GN, bolest minimalnih promjena, pauci-imuni GN i bolest tankih membrana utvrđena u po jednog bolesnika. Svi bolesnici (osim bolesnice s bolesti tankih membrana) liječeni su glukokortikoidima u kombinaciji s ciklofosfamidom, ciklosporinom ili azatioprinom. Zaključno ističemo da je u svih bolesnika s RA potrebna i redovita kontrola bubrežne funkcije a u jasnim indikacijama kompletna nefrološka obrada uz biopsiju bubrega., In rheumatoid arthritis (RA) kidney is commonly affected organ with clinical presentation characterised by proteinuria (often nephrotic range) and microhematuria followed by chronic renal failure. This condition is well recognized as a rheumatoid nephropathy (rheumatoid glomerulonephritis), which is mediated by an immunological inflammation and by nephrotoxic effects of numerous drugs usually used in rheumatoid arthiritis treatment, such as NSAID, DMARD. In the patohistological examination various kinds of associated renal lesions could be seen. The most often are amyloidosis, glomerulonephritis, interstitial nephritis. In this study, we presented 15 patients, 10 women and 5 men, mean age of 60.2 with average rheumatoid arthritis duration of 19.4 years and signs of rheumatoid nephropathy. In all patients renal biopsy was performed with frequency of histopathological findings as follows: amyloidosis in 5 patients, IgA nephropathy in 3 patients, FSGS in 3 patients, mesangial proliferative glomerulonephritis in 3 patients, minimal change disease, pauci-immune glomerulonephritis and thin membrane disease in 1 patient. In all patients (except patient with thin membrane nephropathy) we started immunossuppresive therapy with glucocorticoids in combination with cyclophosphamide or cyclosporin or azatioprine. In conclusion, in all patients with rheumatoid arthritis, parameters of renal function should be monitored and in the case of patologic results, renal biopsy should be be performed. In the treatment of RA patients with related renal disorder, suspected causal drug should be removed from the treatment and specific immunosuppressive therapy initiated.

Stevens-Johnson syndrome mostly involves the skin and mucous membranes. The diagnosis is made when the characteristic rash appears 1 to 3 weeks after exposure to a known stimulus and cannot be explained by some other diagnosis. A 62-year-old woman was admitted for evaluation of toxo-allergic dermatitis and collagenosis. Ten days prior to admission she was taking a course of azithromycin for upper respiratory tract infection. After a few days she was feeling better but maculopapular, erythematous rash developed over her palms, accompanied by fever and chills as well as reddish discoloration around her eyes. Within the next few days the rash progressed to the feet. Routine hematologic, biochemical and immunologic studies did not confirm the diagnosis of inflammatory rheumatic disease. Corticosteroid therapy with methylprednisolone (1 mg/kg) for the presumed Stevens-Johnson syndrome was started and her condition improved in several days; she became afebrile and her skin lesions gradually disappeared. There is only one report, in a child, documenting the association of Stevens-Johnson syndrome with azithromycin, as in this patient.

A 60-year-old male from the Mediterranean area presented with edematous right leg and livid nodules and macules on the skin of upper and lower extremities. Biopsy specimen obtained from the right upper leg showed a pathohistologic finding indicative of Kaposi's sarcoma. Polymerase chain reaction testing revealed HHV-8 in the skin lesion. Serology for HIV was negative. Additional examinations did not reveal dissemination of the disease. Negative HIV serology, normal laboratory findings and absence of immunosuppressant therapy in the patient's history confirmed the diagnosis of the classic form of Kaposi's sarcoma.

A case of a 37-year-old man admitted to our Department of Internal Medicine for medical evaluation of hypertension is reported. The patient had a 4-year history of oscillating hypertension prior to admission, however, with no major subjective complaints, except for pollakisuria. Clinical and biochemical assessment revealed no damage to target organs. Laboratory parameters showed normal values, except for hyperlipidemia. On routine ultrasonography of the pelvis confirmed a pelvic tumor of uncertain etiology, with no abdominal lymph node enlargement. No signs of metastasis were found. The patient was transferred to the Department of Surgery, where the tumor was removed in toto. Histopathologic analysis of the tumor, 11 x 8 x 8 cm in size, composed of cellular and mixoid areas with traces of collagenous connective tissue, necrosis, and tiny calcifications with scattered palisading nuclei and Verocay bodies, pointed to the diagnosis of a benign tumor, i.e. neurilemmoma. Postoperatively, the patient's subjective state was excellent, with normal blood pressure values, and without pollakisuria. A very large space-occupying lesion was responsible for compression of the neighboring organs, especially urinary bladder, resulting in pollakisuria. To our knowledge, pelvic localization of neurilemmoma, particularly a large one, is rare.

The renin-angiotensin-aldosterone system (RAAS) has been considered one of the probable pathophysiologic mechanisms involved in disease progression. Genetic polymorphism of the RAAS has been associated with the clinical course of renal disease. One of the genetic polymorphisms is a deletion or insertion of a 287 base pair fragment in intron 16 of the angiotensin-converting enzyme (ACE) gene. It is known that ACE gene polymorphism is present in humans and that it is associated with an increased risk of cardiovascular diseases, renal disease progression and sarcoidosis. In this study, the potential significance of ACE gene polymorphism in patients with systemic lupus erythematosus (SLE) was investigated. ACE gene polymorphism was determined in 18 patients with SLE and in 21 healthy volunteers as a control group. The mean age of patients was 38.5 years. All patients had a mean follow-up of 30.7 +/- 20.2 months (range 5-95 months). ACE genotypes were determined by the method of polymerase chain reaction. Proteinuria and creatinine were also followed. The frequency of DD, ID and II genotypes was 50%, 28% and 22% in SLE patients and 25%, 50% and 25% in healthy controls, respectively. DD genotype was more common in SLE patients than in the control group. The patients with II genotype had lower proteinuria and creatinine level than those with DD genotype (p < 0.05). The time to disease remission was shorter in patients with II genotype (p < 0.05). Study results indicated an increased frequency of D allele in SLE patients. The increased ACE activity in these patients pointed to the need of further studies of ACE gene polymorphism in SLE.

Anxiolotic effect of BPC-157, a gastric pentadecapeptide: shock probe/buryng test and light/dark test