[Collapsing Glomerulopathy Secondary to Anabolic Steroids for Bodybuilding: A Case Series].

The abuse of anabolic androgenic steroids (AAS) for competitive (and non-competitive) purposes for bodybuilding practice is increasingly common. The consequences of these substances on the various organs are only partially known. Cases of FSGS following the use of AAS have been reported in the literature, even with evolution to ESKD. We describe three cases of bodybuilding athletes who presented alterations in renal function indices after taking AAS for a long time. Three renal biopsies were performed with histological diagnosis of FSGS collapsing variant. We examine the lesions observed on histological examination. Two athletes had rapid progression of renal disease requiring replacement therapy. The third one continues conservative treatment for chronic renal failure. We discuss the risks related to the intake of doping substances and how bodybuilders are exposed to different causes of kidney damage: anabolic steroids, supplements, and a high-protein diet.

Urate-Lowering Agents in Asymptomatic Hyperuricemia: Role of Urine Sediment Analysis and Musculoskeletal Ultrasound.

Current urate-lowering therapy (ULT) includes three direct acting drugs (allopurinol, febuxostat, Rasburicase) and at least four 'indirect' drugs with other important targets (canagliflozin, losartan, fenofibrate and sevelamer). Moreover, the alcalinization of urines using bicarbonate can be used to dissolve urate crystals and the clinician may discontinue several drugs are known to increase serum levels of uric acid, such as diuretics, aspirin, cyclosporine, theophylline, mycophenolate and ACE inhibitors. While there is a consensus to start ULT in cases of symptomatic hyperuricemia (gout, urate-nephrolithiasis), the very frequent conditions of asymptomatic hyperuricemia remains a major conundrum. The effect of asymptomatic hyperuricemia on kidney function has had fluctuating positions over decades. The conflicting results might indicate: (i) the presence of counterbalancing positive and negative effects on kidney function of both serum uric acid and urate-lowering agents, (ii) the presence of a subpopulation of patients, as yet unidentified, which could truly benefit from a urate-lowering therapy. Therefore, today the treatment of asymptomatic hyperuricemia is not recommended nor excluded by current guidelines. Here we suggest that a possible guide for the treatment of asymptomatic hyperuricemia might be the presence of urate crystals in the urine sediment and/or signs of asymptomatic articular damage by urates, identified by musculo-skeletal ultrasound. Moreover, a watchful analysis of the trend in creatinine/eGFR, proteinuria or urate levels might also guide the clinician. Initiation of ULT and follow-up in cases of asymptomatic hyperuricemia should consider urine sediment analysis, musculoskeletal ultrasound and trends in creatinine, proteinuria and serum urate levels.

Ramipril in post-renal transplant erythrocytosis.

BACKGROUND: Posttransplant erythrocytosis (PTE; i.e., hematocrit [Ht] >=51%) may be responsible for cardiovascular events. Angiotensin-converting enzyme inhibitors (ACEIs) are increasingly employed in PTE treatment. Diverse ACEIs have been administered at variable doses and with erratic follow-up. In addition, guidelines recommend the administration of ACEIs as first-line therapy for PTE but do not give information on dosage. In this study the dose-response of a single ACEI was assessed, and patients were followed up for 1 year. The role of ACE gene polymorphism in both prevalence of PTE and successful response to ACEI therapy was also tested. METHODS: At study entry, blood chemistry and ACE-gene polymorphism were measured. ACEI (ramipril) was initiated at 1.25 mg/day; if Ht was still >=51%, ramipril was increased every 6 weeks to ensuing greater dosages. Scheduled dosages were 1.25, 2.5, 5.0, 7.5 and 10 mg/day. Blood chemistry was repeated every 6 weeks. Serum erythropoietin (EPO) concentration was assayed at the start and end of the study. Follow-up was extended for 1 year. RESULTS: PTE developed 12.6 +/- 16.0 months after transplantation in 40 out of 400 patients; 27 patients completed the study. Initial Ht was not correlated with any variable. Final Ht appeared normalized in 26 out of 27 patients. Mean dose (+/- SD) of ramipril was 4.6 +/- 3.6 mg. Mean time for correction of PTE was 135 days, and was not dependent on baseline Ht, hemoglobin or EPO. PTE relapsed in 4 patients. Prevalence of PTE and successful response to ramipril was not dependent on ACE-gene polymorphism. CONCLUSION: Ramipril was effective in PTE; low doses normalized Ht in most patients. No clinical characteristics or biochemical variables predicted the response to ramipril. PTE may relapse; thus long-term follow-up is mandatory.

[Role of directional power-Doppler in the identification of renovascular malformations]. / Ruolo del power-Doppler direzionale nell'identificazione di malformazioni vascolari renali.

OBJECTIVE: The directional power-Doppler (dPD) is a useful tool in evaluating the renal vascularization for its high sensibility and availability. Renal vascular malformations like the arteriovenous fistulas (avF) are rare and their real incidence is unknown. We evaluated the diagnostic role of dpD in renal avF. MATERIAL AND METHODS: From January 1999 to 2002 1518 subjects (875 males, 643 females, mean age: 62 years, range: 22-87 years) have been studied by both B-mode ultrasound and by dpD. All ultrasonographies were taken with a Toshiba Power Vision 6000 by the same skilled operator. RESULTS: Among 1518 patients examined, 17 avF have been identified (diameter range: 3-18 mm) by using dPD. Four of these have an unclear etiology (congenital?) and they have been considered idiopathic. On the contrary, five are acquired: two are caused by renal biopsy, two by renal tumors and one by ureteral stent positioning, respectively. Eight patients, all affected by polycystic kidney disease, showed multiple avF. The four subjects with idiopathic avF are suffering from chronic renal failure (CRF--CrCl = 8-35 ml/min); on the contrary, among patients with polycystic kidney, five of them are on CRF (CrCl = 14-27 ml/min), three have normal renal function. The acquired avF caused by renal biopsy or by ureteral catheterization have spontaneously disappeared after 15-20 days from the causative event. CONCLUSIONS: The dPD allows to individualize the arteriovenous malformations of renal vasculature which could be underestimated or not evidenced by other instrumental methods.