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Background: Numerous studies have explored the role of kidney replacement therapy (KRT) in phosphorus (P) control among prevalent hemodialysis (HD) patients. However, whether the reduction of P achieved during KRT affects parathyroid hormone (PTH) levels is still a matter of debate., Methods: We conducted a retrospective observational study on the prevalent HD population at the Division of Nephrology, University Hospital of Verona, from January to December 2022. We Included clinically stable adult patients undergoing HD for over 6 months, with multiple recorded visits during the follow-up. Demographic, clinical, laboratory, and medication data were collected. Time-varying variables were updated at each study visit. The primary outcome of interest was PTH levels. The absolute intra-HD change in P (intra-HD ∆P), defined as the difference between pre- and post-HD P levels, served as the main exposure. Multivariable adjusted linear mixed models were used to investigate the relationship between intra-HD ∆P and PTH levels., Results: A total of 211 patients contributed to 904 study visits. A significant and positive relationship was observed between intra-HD ∆P and pre-HD P (β = 0.76, 95% CI 0.75, 0.78, p < 0.001) and urea reduction ratio (β = 0.38, 95% CI 0.35, 0.41; p < 0.001). An increase in intra-HD ∆P was significantly and independently associated with low PTH levels (β = - 0.16, 95% CI - 0.30, -0.03; p = 0.020)., Conclusions: The extent of intra-HD P reduction significantly correlates with low PTH levels. Strategies focused on optimizing or enhancing depurative efficiency in KRT can exert a substantial impact on managing positive phosphorus balance and secondary hyperparathyroidism. The assessment of intra-HD P reduction may play a pivotal role in the management and follow-up of secondary hyperparathyroidism in HD patients., (© 2024. The Author(s) under exclusive licence to Italian Society of Nephrology.)

Introduction: Patients with chronic kidney disease on hemodialysis (HD) are at high risk of developing both iron deficiency and iron deficiency anemia (IDA). The administration of intravenous iron therefore represents the standard of care for the management of anemia in this patient setting., Methods: A retrospective cohort of 38 HD patients in Italy was analyzed to assess the clinical and economic implications of switching from intravenous ferric gluconate (FG) to ferric carboxymaltose (FCM) on achievement of adequate hemoglobin (Hb) values and iron balance. The total observational period for each patient was 12 months, 6 months before and 6 months after switching to iron FCM. The pharmacoeconomic analysis considered the hospital perspective and the consumption of iron, blood transfusions and erythropoiesis-stimulating agents (ESAs), including healthcare personnel time., Results: Switching from FG to FCM in dialysis adult patients with IDA allows a cost reduction per patient/month in the range €14-46, considering the use of biosimilar ESA or originator ESA, respectively. The percentage of patients with Hb target values increased from 63% to 82%, considering the entire observation period. In addition, other clinical parameters (ferritin, transferrin saturation, erythropoietin resistance index) improved after switching from FG to FCM., Conclusion: FCM in HD patients was shown to provide a favorable efficacy profile over FG, with a lower cost per patient, mainly driven by a consistent reduction of ESA consumption., Funding: Vifor Pharma Italia Srl.

Background and Objectives: This study examined predictors of the annual decline in estimated GFR (eGFR) in patients with type 2 diabetes and preserved kidney function., Design, Setting, Participants, & Measurements: In a prospective, observational cohort study, 1682 individuals with type 2 diabetes and baseline eGFR ≥60 ml/min per 1.73 m(2) (as estimated by the Chronic Kidney Disease Epidemiology Collaboration equation) were followed for 10 years. Linear regression was used to estimate participants' changes in eGFR over time., Results: During follow-up, 263 (15.6%) individuals had a rapid eGFR decline defined as >4.0% per year. Average eGFR decline was -5.8 ± 3 and -0.6 ± 2 ml/min per 1.73 m(2) per year in rapid decliners and nondecliners, respectively. Compared with normotensive, normoalbuminuric patients (-0.2 ± 0.2 ml/min per 1.73 m(2) per year), those with hypertension (-1.0 ± 0.1 ml/min per 1.73 m(2) per year), hemoglobin A(1c)≥7% (-1.0 ± 0.1 ml/min per 1.73 m(2) per year), longer diabetes duration (-1.0 ± 0.1 ml/min per 1.73 m(2) per year), obesity (-1.2 ± 0.1 ml/min per 1.73 m(2) per year), insulin treatment (-1.5 ± 0.1 ml/min per 1.73 m(2) per year), microalbuminuria (-1.3 ± 0.2 ml/min per 1.73 m(2) per year), or macroalbuminuria (-2.7 ± 0.4 ml/min per 1.73 m(2) per year) had significantly faster age-adjusted annual eGFR declines. Multivariable linear regression analyses revealed that albuminuria (P<0.001) was the strongest predictor of annual eGFR decline. Other independent predictors of annual eGFR decline were older age, hypertension, insulin treatment, and lower baseline eGFR., Conclusions: Annual eGFR decline is predicted by multiple modifiable risk factors in patients with type 2 diabetes and preserved kidney function.

Objective: Recent studies have suggested an association between hyperuricemia and adverse renal outcomes in nondiabetic populations. Data on the relationship between hyperuricemia and the risk of incident chronic kidney disease (CKD) in type 2 diabetic patients with normal or near-normal kidney function are lacking. We determined whether baseline serum uric acid levels predict the subsequent development of CKD in patients with type 2 diabetes., Research Design and Methods: We followed 1,449 type 2 diabetic patients with normal kidney function and without overt proteinuria for 5 years for the occurrence of incident CKD (defined as overt proteinuria or estimated glomerular filtration rate [eGFR] <60 mL/min/1.73 m(2))., Results: During a 5-year follow-up period, 194 (13.4%) patients developed incident CKD. The cumulative incidence of CKD was significantly greater in patients with hyperuricemia than in those without hyperuricemia (29.5 vs. 11.4%, P < 0.001). In univariate logistic regression analysis, the presence of hyperuricemia roughly doubled the risk of developing CKD (odds ratio [OR] 2.55 [95% CI 1.71-3.85], P < 0.001). After adjusting for age, sex, BMI, smoking status, diabetes duration, systolic blood pressure, antihypertensive treatment, insulin therapy, HbA(1c), eGFR, and albuminuria, hyperuricemia was associated with an increased risk of incident CKD (adjusted OR 2.10 [1.16-3.76], P < 0.01). In continuous analyses, a 1-SD increment in the serum uric acid level was significantly associated with a 21% increased risk of CKD., Conclusions: In type 2 diabetic individuals with preserved kidney function, hyperuricemia seems to be an independent risk factor for the development of incident CKD.

The mortality rate in diabetics with chronic kidney disease (CKD) is seven times higher than end-stage renal disease mainly because of cardiac causes. Anaemia may have a relevant role in the pathogenesis of cardiovascular (CV) disease in CKD. Anaemia occurs at an earlier stage of CKD in diabetic individuals than in those with other causes of CKD. Observational findings support the unfavourable influence of anaemia on mortality in CKD patients, and the combination of anaemia and CKD in diabetics identifies a group with a particularly high mortality risk. While the effect of erythropoietin on these patients' quality of life is known, its impact on mortality and CV risk is uncertain. The recent Anaemia Correction in Diabetes (ACORD) trial in diabetic CKD patients, which targeted haemoglobin levels of 13-15 mg/dl, disclosed no statistically significant favourable or adverse effects on mortality or morbidity over the 2-year follow-up, while other studies endeavouring to nearly normalize haemoglobin have reportedly proved risky. Even if anaemia is causally involved, the pathogenesis of CV disease in diabetics with CKD is so complex that addressing just one factor (anaemia) may not suffice to prevent CV risk, and normalizing haemoglobin levels may even be harmful.

Dedicated European and US clinical guidelines for type 2 diabetes in the elderly have been released, but they do not specifically address the issue of advanced chronic kidney disease (CKD) in older patients with diabetes. General clinical guidelines have been published on the treatment of patients with diabetic nephropathy (DN), but these address the issue of how to prevent progression and treat advanced DN without distinguishing between different age groups. Elderly patients with diabetes and stages 3 to 4 CKD have particular needs that differ from those of younger patients with the same conditions. This is mainly due to their frailty and shorter life expectancy. Differently tailored therapeutic strategies are needed, which may have less stringent targets; and the use of common drugs should be critically evaluated. The management agenda (metabolic control, low-protein diet, controlling BP, preventing progression of advanced DN, preventing cardiovascular outcomes) for these patients is discussed in light of the limits and perspectives of current guidelines. Intensive, simultaneous management of all items on the agenda may not be feasible for a proportion of older patients, and clinicians may have to give priority to reducing some risk factors rather than others, choosing between different therapies.

Immunosuppressed organ allograft recipients are at risk of developing lymphomas and lymphoproliferative disorders as a consequence of immunosuppressive therapy and long-term antigenic stimulation from both the graft and possible viral infections. No more than 4% of the malignant tumors detected in organ recipients are plasmacytomas. Primary cutaneous plasmacytoma is a rare type of cutaneous B-cell lymphoma arising primarily in the skin. It is derived from clonally expanded plasma cells with various degrees of maturation and atypia. We report the occurrence of a solitary cutaneous plasmacytoma in a 56-year-old male patient undergoing hemodialysis after rejection of a grafted kidney. The diagnosis was made a few months after the kidney had been surgically removed. A thorough examination showed no evidence of systemic disease. Skin lesions were successfully treated with local radiotherapy. After 2 years of follow-up there were no local or systemic recurrences.

Background: Extramedullary plasma cell dyscrasias are rare., Case Report: We report a case of a 56-year-old male Caucasian hemodialysis patient with cutaneous plasmacytoma. The diagnosis was made a few months after surgical removal of his renal graft due to chronic rejection. Investigations for the presence of an associated myeloma were negative. He underwent local radiotherapy with complete resolution of the skin lesion., Conclusions: Nephrologists should be aware that the frequency of post-transplant lymphoproliferative disorders is increasing in the dialysis population, especially in those previously or currently treated with immunosuppressive drugs.

Background: Cardiovascular risk factors are common findings in uraemics, but the impact of each single factor on the development of atherosclerosis is still a matter of debate., Patients and Methods: In order to evaluate the relationship between diabetes and ischaemic heart disease (IHD) in uraemia, we carried out a retrospective study comparing the results of 33 coronary angiographies performed in non-diabetic patients with those of 13 diabetics (2 had type 1 diabetes, 8 were treated with insulin, 2 with sulfonylureas and 3 received no therapy). Coronary angiography was performed in 29 patients awaiting kidney transplantation and in 17 subjects with IHD., Results: Age, sex, length of time on renal replacement therapy, smoking history, clinical diagnosis of cerebrovascular and peripheral vascular disease, systolic blood pressure (BP), cholesterol, triglycerides, calcium, phosphate, albumin and degree of anaemia were comparable in the two groups. On the contrary, frequency of IHD (77 vs. 30%, p<0.01) and atrial fibrillation (23 vs. 3%, p<0.05) were higher, while diastolic BP (79 +/- 7 vs. 85 +/- 8 mmHg, p<0.05) and calcium phosphate product (47 +/- 10 vs. 57 +/- 15 mg2/dL2, p<0.05) were lower in diabetics than in non-diabetics. Stenotic lesions of the three major coronary arteries were more prevalent in diabetics than in non-diabetics (left anterior descending artery (LAD) 100 vs. 48%, p<0.01; right coronary artery (RCA) 77 vs. 39%, p<0.05; left circumflex artery (LCA) 69 vs. 24%, p<0.01) and in the same way diabetics showed higher narrowing percentage (LAD 74 +/- 30 vs. 30 +/- 36%, p<0.01; RCA 71 +/- 41 vs. 26 +/- 38, p<0.01; LCA 41 +/- 38 vs. 15 +/- 29, p<0.05)., Conclusions: Our study demonstrates that although the uraemic milieu is a risk factor for IHD, diabetes increases the degree of atherosclerotic vascular damage independently of the other cardiovascular risk factors.

Prevalence of cardiovascular disease is high in diabetic patients on renal replacement therapy (RRT); therefore we examined the role of diabetes mellitus on determining the degree of coronary artery stenosis. Twenty-five patients underwent coronary angiography, 12 were awaiting kidney transplantation and the examination was performed regardless of cardiac symptoms, 13 were affected by ischaemic heart disease (IHD). Diabetic and nondiabetic status together with the other risk factors for cardiovascular disease such as age, sex, length of time on RRT, smoking and elevated phosphorus levels history, clinical diagnosis of IHD, cerebrovascular and peripheral vascular disease, mean blood pressure, cholesterol, triglycerides, calcium, phosphate, albumin, haemoglobin, haematocrit and weekly dose of erythropoietin were derived from clinical records. All investigated parameters were matched in diabetic (group 1, n=10) and nondiabetic patients (group 2, n=15) and showed no differences. Clinical evidence of IHD was detected in 80% of patients in group 1 and 46% in group 2 and the percentage of patients on the renal transplant waiting list was not statistically different in the two groups (30 vs 60%). In 60% of patients in group 1 there were 3 or more stenotic lesions equal or greater than 75% of normal reference segment in the major coronary arteries, whilst in 53% in group 2 there were no haemodynamically significant narrowings. Narrowing percentage of the coronaries in group 1 and 2 were: right coronary artery 83 +/- 30 vs 32 +/- 41 (p<0.05), left anterior descending artery 80 +/- 25 vs 44 +/- 34 (p<0.05), left circumflex artery 46 +/- 37 vs 18 +/- 29 (p=0.05) respectively. Our study confirms that IHD is a clinical feature of uraemic diabetic patients and that diabetes is the main cardiovascular risk factor for determining the degree of coronary stenosis.

Mesenteric infarction is increasingly observed in uremic elderly patients with widespread atherosclerosis. A 77-year-old man on renal replacement therapy since June 1997 was admitted because of abdominal pain. The surgical diagnosis was massive intestinal infarction and the patient died a few hours later. A colonoscopy had been performed a few weeks before and a well-limited necrosis of the caecum mucosa had been detected. Hypotensive episodes were frequent during his hemodialysis sessions. In this work we discuss age, symptoms, laboratory investigations, risk factors and the evolution of case reports published during the last few years. Nephrologists should take into account the possibility of mesenteric ischemia in uremic patients with manifest arterio-occlusive disease, abdominal pain and leukocytosis, especially if hypotension is the major complication of the hemodialysis sessions.

The onset of renal damage in diabetes mellitus may be influenced by several factors which largely result from genetic predisposition, hereditary factors and the early appearance of microalbuminuria and/or systemic hypertension. Most of these factors are also implicated in the progression of nephropathy from microalbuminuria to overt proteinuria and to end-stage renal failure (ESRF). Over the last few years, the role of hyperglycaemia has emerged as critical in mediating the progressive renal damage in diabetes. However, hyperglycaemia leads to increased formation of glycated proteins which may act as promoters of progression by localizing in renal tissue. In addition, hyperglycaemia may have a synergistic effect with some other risk factors, such as growth factors and the renin angiotensin system, in accelerating renal deterioration.

Twelve patients (7 men and 5 women) with an average age of 53 years (range 37-69) were hospitalized for renal stones and found to have primary hyperparathyroidism. Five were hypertensive and 7 normotensive. The systemic hemodynamics, plasma renin activity and glomerular filtration rate were evaluated before and at least 6 months after removal of a parathyroid adenoma. After surgery the mean intra-arterial blood pressure fell in almost all patients, due to some reduction in the peripheral vascular resistance index with no change in the cardiac index. However, the hemodynamic variations were not uniform in all patients. No change was seen in plasma renin activity and glomerular filtration rate. A positive correlation between the percent change in mean arterial pressure and percent decrease in total serum calcium was found. The results obtained indicate that it is likely that hypercalcemia plays some role both in patients with high and those with normal blood pressure. The systemic hemodynamic changes after parathyroidectomy indicate that the fall in peripheral vascular resistance could have a certain influence.

Timolol, a non-cardioselective beta-blocking agent, was administered orally after 2 weeks of placebo to 14 patients with essential hypertension for 8 weeks following 1-4 weeks of dose-ranging period. Patients were first hospitalized and submitted to a diagnostic workup. They were placed on a diet containing 100 mEq of Na+ and 65 mEq of K+; this regimen was also prescribed during outpatient treatment. The changes in blood pressure, systemic hemodynamics, plasma renin activity, urine aldosterone, and glomerular filtration rate were evaluated. A significant and stable decrease in systolic and diastolic blood pressure associated with a fall in cardiac output (-21%), heart rate (-17%), plasma renin activity, and urine aldosterone were observed. The blood pressure lowering effect was unrelated to the decrease in cardiac output and plasma renin activity. Glomerular filtration rate was unchanged. No important side effects were observed during the treatment.

A clinical study was performed in 2 groups of patients with solitary kidneys, followed for 11-146 months. Group 1 had 9 patients (7 males and 2 females, aged between 23 and 68 years) with unilateral renal agenesis. Group 2 had 13 patients (9 females and 4 males, aged between 27 and 70 years) who underwent unilateral nephrectomy for the following reasons: hydronephrosis secondary to ureteropelvic junction stenosis, 7 patients; renal trauma, 4 patients; benign neoplasia, 2 patients. During the follow up, urinary protein excretion of more than 300 mg/day was observed in 9 patients, 3 in group 1 and 6 in group 2. Eleven patients, 8 in group 1 and 3 in group 2, were hypertensive (diastolic blood pressure higher than 95 mm Hg). Hyperuricemia was observed in 14 patients, 10 in group 1 and 4 in group 2. Seven patients, 4 in group 1 and 3 in group 2, had a significant deterioration of renal function. Neither proteinuria nor renal failure were observed before at least 10 years had elapsed since the anatomic condition of solitary kidney had been established. A surgical renal biopsy was performed in 1 patient with unilateral renal agenesis and showed focal glomerular sclerosis. This study adds support to the view that the reduction of 50% of the renal tissue may be a risky situation in humans as well as in animals.

The frequency of renal tubular acidosis was evaluated in 28 adult patients with recurrent calcium nephrolithiasis (19 with 'renal' hypercalciuria, 9 with normocalciuria and no metabolic abnormality) and no evidence of obstruction or infection of the urinary tract. Eight patients with hypercalciuria (42%) had a defective renal reabsorption of bicarbonate, based on a fractional excretion of bicarbonate higher than 7% and a TmHCO3/GFR lower than 2.2 mEq/dl; 2 of them had an associated distal defect of acidification, as judged by a U-B pCO2 lower than 18 mm Hg in maximally alkaline urine. One patient with hypercalciuria had distal tubular acidosis, based on a urine pH higher than 5.3 during acidosis. Only 1 patient with normocalciuria had associated proximal and distal acidification defects. The remaining 8 patients displayed a normal renal acidifying capacity. The bicarbonate wastage was independent of serum PTH levels, vitamin D status and hypercalciuria and was associated with a defective tubular reabsorption of phosphate, increased random urinary pH and more active nephrolithiasis, with a prevalence of mixed calcium oxalate and phosphate stones. Our study shows a high incidence of defective tubular reabsorption of bicarbonate in patients with calcium nephrolithiasis and 'renal' hypercalciuria and suggests that the proximal acidification defect plays a pathogenetic role in promoting calcium nephrolithiasis.

32 polycystic kidney disease (PKD) patients, 16 with normal 16 with variably decreased renal function, were studied; 12 were normotensive, 20 were hypertensive. Mean arterial pressure (MAP) was 90 +/- 8 mm Hg in the normotensive group and 117 +/- 17 in hypertensive patients; plasma renin activity (PRA) was similar. The glomerular filtration rate (GFR) was lower, but not significantly, in the hypertensive group and plasma volume (PV) was higher in hypertensive patients (normotensive 40.25 +/- 3.47 ml/kg body weight; hypertensive 46.30 +/- 3.54). No correlation was found between MAP, and PRA or GFR but MAP correlated with PV. Cardiac output was higher in hypertensive patients (normotensive 3.48 +/- 0.70 l/min/m2; hypertensive 3.89 +/- 1.47), also total peripheral resistance was higher in the hypertensive group (normotensive 2,035 +/- 503 dyn/s/cm-5/m2; hypertensive 2,577 +/- 808). Cardiac output and PV showed a high degree of correlation, but no correlation was seen between total peripheral resistance and PV, or PRA. The hypertensive patients were divided into two groups: one with hypertension of less than 2 years duration and one with more than 2 years but with similar GFR, PRA, PV and hemodynamic pattern. Our data indicate that hypertension in PKD is volume-dependent; that the increase in PV was not related to the loss of GFR, and that the role of the renin-angiotensin system in maintaining the hypertensive state is not well defined. Hemodynamically hypertension is characterized by high cardiac output and total peripheral resistance independent of the duration of hypertension.