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We conclude that intravenous conivaptan is an effective aquaretic to treat hyponatraemia caused by SIADH, as evidenced by a simultaneous increase in serum sodium and decrease in urine osmolality. Baseline values of serum sodium, blood urea nitrogen and estimated glomerular filtration rate may help predicting the magnitude of response to therapy.

BackgroundAdrenocorticotropic hormone is being increasingly studied for treatment of various glomerulopathies, most notably membranous nephropathy. Less data are available regarding its use in idiopathic nephrotic syndrome (INS) secondary to minimal change disease (MCD) or focal segmental glomerulosclerosis (FSGS). We report here our experience with H.P. Acthar® Gel (repository corticotropin injection) as first-line or subsequent therapy in patients with INS.MethodsData were taken from three patients with MCD and ten patients with FSGS from around the US, who were treated with Acthar Gel as initial or subsequent therapy. Treatment was solely at the discretion of the primary nephrologist without a specific protocol. A complete response (CR) was defined as final urine protein-to-creatinine ratio <500 mg/g and a partial response (PR) as 50% decrease without rise of serum creatinine. Side effects and tolerability were noted.ResultsAll three patients with MCD received Acthar Gel as second-line or later immunosuppressive (IS) therapy and all responded (one CR and two PRs). Two of the ten patients with FSGS received Acthar Gel as first-line IS therapy, while the other eight had failed multiple agents. Four of the ten patients with FSGS had responses, including two CRs and two PRs. The three patients with MCD tolerated therapy well without side effects. Five patients with FSGS tolerated therapy well, while five had various steroid-like side effects, resulting in therapy discontinuation in two patients.ConclusionActhar Gel is a viable alternative IS agent for treatment of INS in patients intolerant or resistant to conventional therapy. More data are needed to better define its appropriate place.

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The kidney is a target organ in thrombotic thrombocytopenic purpura (TTP), but the pattern of proteinuria has been poorly described. We retrospectively analyzed proteinuria in all 59 patients with a diagnosis of TTP on their discharge summary from 2000 to 2009. Urinalysis was obtained in 89% of cases; in those, proteinuria was detected by urine dipstick in 85%. In patients with dipstick proteinuria, quantification (grams per day or grams per gram creatinine) was performed in only 34% and ranged from 0.16 grams to 8.0 grams. Patients with larger amounts of proteinuria had more severe acute renal failure, were more likely to receive a renal biopsy, and were more likely to undergo dialysis. When analysis was restricted to patients with highly depressed activity levels of the metalloprotease ADAMST13, proteinuria tended to be low grade and transient, and renal insufficiency was mild. Proteinuria is common in thrombotic microangiopathies and may be nephrotic-range, but TTP with depressed ADAMST13 activity is characterized by less proteinuria and less severe renal dysfunction. Although this study presents the largest sample of proteinuria quantification ever reported for TTP, quantification was performed in only one-third of cases