The appearance of renal failure during episodes of macroscopic hematuria (EMH) in IgA nephropathy (IgAN) has been described as very unusual. The results of a prospective investigation on the effect of EMH on renal function in IgAN are presented. During a 3-year period, 29 episodes of EMH occurring in 21 patients with IgAN have been studied. A derangement of renal function (increase of serum creatinine by more than 0.5 mg/dl) was observed in 11 episodes (37.9%) with peak creatinine values ranging from 1.2 to 6.7 mg/dl. The worsening of renal function was accompanied by a longer duration of EMH (4.8 +/- 1.3 vs. 3.5 +/- 1.5 days; P less than 0.05) but not by arterial hypertension or edema. A complete recovery of renal function was observed in every patient 1 to 2 months after the start of EMH. The histological survey disclosed that the decrease of renal function correlated closely with the presence of red blood cell casts in as much as 50% of the tubular lumen and with findings of tubular necrosis. We conclude that a worsening of renal function can be observed frequently during the EMH. Tubular damage and obstruction by red blood cell casts may play a significant role in the pathogenesis of this complication.
We describe the long-term follow-up of severe lupus nephritis treated with cyclophosphamide, with emphasis on the incidence of relapses after therapy withdrawal. From a cohort of SLE patients followed over a period of twelve years, we review the charts of the eleven with histologic evidence of class IV nephritis who reached complete remission with cyclophosphamide and who were followed for more than four years after the discontinuation. In all patients, cyclophosphamide was maintained for longer than two years after complete remission. Four patients relapsed following therapy withdrawal (36%). Sequential biopsies were taken in eight patients after remission or relapse and show a good histologic correlation with clinical renal data. Clinical remission with re-induction therapy could not be achieved in two patients after relapse. We conclude that relapse is frequently observed following cyclophosphamide withdrawal in lupus patients with diffuse proliferative glomerulonephritis initially responsive to this therapy. Studies are needed to determine the influence of different regimes of maintenance therapy on the rate of relapses.
We have prospectively studied 37 adult patients (15 males, 22 females; age 31 +/- 10.6 years) with previously undiagnosed isolated hematuria in which hypercalciuria or hyperuricosuria was found. Eighteen of them had had episodes of gross hematuria. Isolated hypercalciuria (4.4 to 10.4, X 5.6 +/- 1.9 mg/kg/24 hr) was found in nine patients (Group I), isolated hyperuricosuria (784 to 1500, X 1088 +/- 228 mg/24 hr) in 11 (Group II), and both hypercalciuria (4 to 8, X 4.9 +/- 1 mg/kg/24 hr) and hyperuricosuria (752 to 1476, X 1042 +/- 181 mg/24 hr) in 17 patients (Group III). Thiazide treatment for patients with hypercalciuria and allopurinol for those with hyperuricosuria were administered; calciuria and uricosuria became normal by the first month of therapy in every case. In 22 (59.4%) cases (Responder patients) hematuria resolved completely as soon as calciuria and uricosuria became normal. In the remaining 15 cases (Nonresponder patients) hematuria persisted despite the normal calcium and uric acid excretions. Several disorders that explained hematuria were diagnosed later in most of Nonresponder patients. Responder patients persisted without hematuria on the follow-up; only in three patients a transient relapse of hematuria was seen associated with a sudden increase of calciuria and uricosuria because of treatment withdrawal. There were no differences in age, male/female ratio nor in the basal values of calciuria and uricosuria between Responder and Nonresponder patients. A familial history of urolithiasis was found more frequently in Responder patients (64%) than in Nonresponders (20%) (P less than 0.05). We conclude that hypercalciuria and hyperuricosuria are definable and potentially reversible causes of hematuria in adult patients.
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