Plasmapheresis for crescentic IgA nephropathy: a report of two cases and review of the literature.

Idiopathic IgA nephropathy is widely regarded as a slowly progressive disease that not infrequently results in end-stage renal failure. Only a minority of patients present with either a rapidly progressive form of glomerulonephritis, or with end-stage renal failure. Anecdotal reports of improved renal function after treatment with plasmapheresis have been published, but the efficacy of this therapy remains controversial. We describe the course of two young males presenting with uremia, hypertension, nephrotic-range proteinuria, and crescentic glomerulonephritis on renal biopsy. Both patients underwent therapy with steroids, immunosuppressive agents, and plasmapheresis without an appreciable improvement in renal function. A review of the literature does not offer any conclusive data to support the role of plasmapheresis in the treatment of rapidly progressive glomerulonephritis due to IgA nephropathy and points out the need to define criteria that may identify subsets of patients with this disorder who may potentially benefit from plasma exchange therapy. J. Clin. Apheresis 14:185-187, 1999. Published 1999 Wiley-Liss, Inc.

Resolution of proteinuria secondary to bilateral renal vein thrombosis after treatment with systemic thrombolytic therapy.

A case of significant proteinuria occurred as a result of bilateral renal vein thrombosis secondary to dehydration, which resolved after treatment with urokinase. The patient developed nausea and vomiting from viral gastroenteritis with subsequent volume contraction. He later noted the onset of aching lower abdominal and flank pain. On admission, he was noted to have a serum creatinine of 1.7 mg/dL, and 4+ proteinuria on urinalysis. A 24-hour urine collection showed 2.34 g protein. A renal venogram showed bilateral renal vein thrombosis (RVT) without involvement of the inferior vena cava. Therapy was initiated with heparin at 1,000 U/hr, followed by intravenous (IV) urokinase, 4,400 U/kg bolus, followed by 4,400 U/kg/hr with continuous infusion for 12 hours. A repeat renal venogram done at this time showed partial resolution of thrombosis bilaterally. A second 12-hour infusion of urokinase at 5,000 U/kg/hr was performed; at this time, the patient reported resolution of his flank and abdominal pain. A repeat 24-hour urine collection showed 60 mg protein with a normal creatinine clearance. Levels of antithrombin III, protein C, and protein S were all normal. A renal biopsy was performed and showed normal histology on light, immunofluorescent, and electron microscopic evaluation. The patient has done well on no therapy and has had no recurrence of thrombosis or proteinuria after 2.5 years. This is a US government work. There are no restrictions on its use.

Where the kidney is concerned, how much mannitol is too much?

OBJECTIVE: To report a case of mannitol-induced acute renal failure (ARF). CASE SUMMARY: A 31-year-old woman who had been on long-term warfarin therapy for atrial fibrillation was admitted to the hospital with hemoptysis. Following reversal of her anticoagulation, she had a tonic-clonic seizure nine days after admission. An emergency computed tomography scan revealed cerebral edema, which was initially treated with hyperventilation and steroids. Two days later, a repeat scan showed progression of the cerebral edema with midline shift. Mannitol 550 g was infused over the next 28 hours, precipitating ARF. Despite prompt hemodialysis to reverse the renal failure, the patient died. This case of apparent mannitol-induced ARF illustrates several pathophysiologic effects of this agent. DISCUSSION: Case reports in the literature discussing mannitol-induced ARF are reviewed and compared. A relationship between dose and ARF and its reversal with hemodialysis is postulated. CONCLUSIONS: It is likely that sufficient doses of mannitol may lead to ARF. Limitation of dose may prevent and treatment with hemodialysis may reverse ARF in these instances.

Treatment of digoxin intoxication in a renal failure patient with digoxin-specific antibody fragments and plasmapheresis.

A patient with renal failure due to myeloma kidney and coincident digitalis intoxication due to prescribed daily digoxin administration was treated with digoxin-specific antibody fragments and plasmapheresis. Rapid response to therapy was noted, removal of digoxin-antidigoxin antibody complexes was confirmed, and prevention of delayed rebound toxicity was documented. We suggest that this is the therapy of choice in similar individuals.

Bilateral renal artery stenosis: presenting as a case of scleroderma renal crisis.

A patient with long-standing scleroderma who developed malignant hypertension is presented. Renal insufficiency aggravated by the use of angiotensin-converting-enzyme inhibition prompted renal angiography. The latter demonstrated bilateral renal artery stenosis, an uncommon coexistence of two infrequent disorders.

Thrombotic thrombocytopenic purpura in human immunodeficiency (HIV)-seropositive males.

Two male patients with thrombotic thrombocytopenic purpura (TTP) were found to have antibodies to the human immunodeficiency virus (HIV). In one patient, platelet-associated antibody levels were measured serially and were found to be initially elevated, but the levels decreased with initiation of successful therapy. The simultaneous occurrence of these two conditions in two of three patients admitted for TTP within the previous 2 years at this institution suggests an association between the two diseases. The precise nature of this association remains speculative inasmuch as the pathogenesis of TTP remains uncertain.

Crescentic glomerulonephritis complicating idiopathic membranous glomerulonephropathy.

We describe the course of a patient with multiple rectal abscesses and progressive renal dysfunction. A renal biopsy demonstrated a membranous glomerulopathy associated with extensive crescent formation. No underlying cause for the glomerulonephritis could be identified and, specifically, the anti-GBM antibody present in other similar cases was not found. There appears to be a subset of patients with membranous glomerulopathy in whom crescents develop with rapid loss of renal function. Anti-GBM antibody is not necessary in the pathogenesis of this lesion.