Clinicopathological study of poststreptococcal glomerulonephritis in the elderly.

In order to characterize the clinical features in elderly patients with poststreptococcal glomerulonephritis (PSGN), 31 patients, who were both histologically and immunologically proven to be PSGN, were divided up into 3 groups according to age; elderly patients being 55 years or older (n = 7), middle-aged patients being 40 to 54 years old (n = 7) and younger patients being 20 to 39 years old (n = 17). Renal functional impairment as indicated by serum creatinine levels of over 2.0 mg/dl, developed in 4 of the elderly patients and later completely improved at the end of the follow-up period (178.9 +/- 150.7 days). On the other hand, none of the middle-aged and younger patients revealed any renal function impairment. Hypertension was observed more frequently in elderly patients than in younger patients, and was 86% and 6% at the time of admission, respectively. In addition, 43% of elderly patients remained hypertensive at the time of discharge. There was no difference in total protein, ASO, CH50, the degree of proteinuria or proliferative and exudative features in renal histology among the three groups. None of the elderly patients with PSGN died or developed persistent renal failure. In conclusion, elderly patients with PSGN had a high incidence of renal functional impairment and hypertension compared to the younger patients on admission, however, their short-term prognosis seems to be favorable.

Captopril-induced metabolic acidosis with hyperkalemia.

Hyperreninemic hypoaldosteronism was diagnosed in a 34-year-old woman with hypertension who was receiving captopril therapy. Renal biopsy revealed an advanced stage of IgA nephropathy, and her creatinine clearance was 40 ml/min. Elevation of serum potassium from 4.7 to 5.8 mEq/l and development of hyperchloremic metabolic acidosis with laboratory findings of pH 7.285, HCO3- 13.5 mEq/l, Na 141, and Cl 114 mEq/l were observed after captopril therapy. When captopril was withdrawn, elevated serum potassium levels and metabolic acidosis returned to normal. Challenge with captopril resulted in a decrease in plasma aldosterone levels, an increase in plasma renin activity, and development of hyperkalemic, hyperchloremic metabolic acidosis which is corrected with mineralocorticoid replacement. This case study demonstrates that captopril can cause hyperreninemic hypoaldosteronism with the laboratory finding of hyperkalemic, hyperchloremic metabolic acidosis.

Glomerulocystic kidneys. Report of an adult case.

Glomerulocystic kidney characterized by dilatation of Bowman's space occurs primarily in infants and children. We treated a normally developed 29-year-old Japanese man for hypertension and renal failure, who had been well up to 6 months before admission. Extrarenal malformations were not determined. A biopsy of both kidneys was done at the time of interdialysis, and the histology revealed diffuse glomerular cystic lesions. Electron-dense deposits were also observed in the mesangial area. Radiological studies of the kidneys showed numerous minute cysts in the cortical area, a normal architecture of the arterial trees, and negative evidence of urinary tract obstruction. This may be the first documentation of glomerulocystic kidney in an adult, without extrarenal anomalies.

Pharmacokinetics of a new angiotensin I converting enzyme inhibitor (alacepril) after oral dosing in fasting or fed states.

The plasma concentration and urinary excretion of a newly developed angiotensin I converting enzyme inhibitor, alacepril (which is converted to captopril after absorption), were investigated in seven normal healthy subjects. Fifty milligrams of the drug was administered orally either in the fasting or in the fed state. In the fasting state, the time of maximal plasma concentration (tmax) was 1 hour for free captopril, 1.7 hours for protein-conjugated captopril, and 1.6 hours for total captopril. The biologic t1/2 of free, protein-conjugated, and total captopril was 1.9, 4.2, and 5 hours, respectively. In the fed state, neither tmax nor t1/2 changed, except that the tmax of free captopril was prolonged to 1.9 hours (P less than 0.01). Cumulative urinary excretion of free captopril at 8 hours was 35% of the drug administered in the fasting state and that of total captopril at 24 hours was 59%. These data did not differ significantly from those obtained after food intake. The biologic t1/2 of free captopril after alacepril dosing was longer than in previous studies of captopril per se. Because biologic or clinical effects have not been studied, it should be left conjectural whether alacepril is a longer-acting angiotensin I converting enzyme inhibitor. A prolonged effect of the drug can be expected by its administration after a meal.