A patient with severe idiopathic hyperuricemia and hypokalemic alkalosis was followed over a one-year period. A tubulointersitial nephritis consistent with hypokalemic nephropathy was found on biopsy. However, the possibility that the hyperuricemia contributed to the hypokalemia and renal lesion cannot be excluded. Inappropriate urinary loss of potassium could be prevented by administration of spironolactone or triameterene. Six months after initiation of allopurinol therapy with reduction of serum uric acid concentrations to normal concentrations, this potassium wasting was substantially decreased.

Adult↗

PubMedDate not supplied

Hypokalemia: causes, consequences and correction.

Hypokalemia poses a common diagnostic challenge with many potential etiologies. Multiple factors may contribute to this electrolyte deficiency in any given patient. Gastrointestinal potassium wasting usually is identifiable by an associated increase in fluid losses via biliary tract or bowel. A urinary potassium excretion of 20 mEq or more per day in the presence of a low serum potassium (less than 3.5 mEq/L) suggests inappropriate potassium wasting. Although diuretic therapy (loop diuretics, thiazides) undoubtedly is the most common cause of a potassium deficit, one also must consider abnormalities of the pituitary-adrenal axis, renal disorders including tumors, other drugs, and a variety of less well-defined entities. Potassium deficiency may produce both functional and structural defects in the kidneys, myocardium, skeletal muscle, central nervous system, and gastrointestinal tract. Treatment is aimed at replacing potassium intravenously or orally or preventing further potassium loss (spironolactone, triamterene); when associated with a metabolic alkalosis (chloride deficiency), the replacement should be potassium chloride.

Acidosis, Renal Tubular↗

PubMedDate not supplied

An etiology of nephrotic syndrome in chronic interstitial nephritis (pyelonephritis); an electron microscopic study.

Renal tissues were studied using electron microscopy (EM) and immunofluorescence microscopy (IFM) from three patients who were found to have chronic interstitial nephritis (pyelonephritis) by light microscopy (LM). By LM, 90% of the glomeruli in two patients and all glomeruli in one patient were normal. By EM, glomerular capillaries in all patients revealed generalized fusion of epithelial foot processes. In two patients, IFM for immunoglobulins, third component of complement and fibrinogen were negative. These two patients received corticosteroids for 6 to 12 weeks. In one, proteinuria markedly decreased (from 17.9 to 1.1 gm) in four weeks and in the other follow-up studies of renal histology revealed normal glomeruli and partial restoration of foot processes by LM and EM respectively. Thus, this study offers evidence for lipoid nephrosis (or minimal lesion disease) as an etiology of nephrotic syndrome in chronic interstitial nephritis (pyelonephritis). The impaired renal function in these patients is attributed to tubulo-interstitial disease rather than glomerular pathology. It remains to be determined whether the two disparate pathological conditions have coexisted or chronic interstitial nephritis had led to the appearance of lipoid nephrosis through an unidentified mechanism.

Adult↗