We studied the relative importance of hyperkalemia and mineralocorticoid deficiency in the metabolic acidosis of a patient with proved isolated hyporeninemic hypoaldosteronism and moderate kidney failure. The hyperkalemia and acidosis were severe in relation to the slight azotemia. Despite the systemic acidosis and urinary pH of 4.9, urinary ammonium excretion was distinctly blunted. Correction of the hyperkalemia by potassium-sodium exchange resin alone resolved the acidosis and restored the previously diminished urinary ammonium excretion to normal. Administration of mineralocorticoids only partially corrected the hyperkalemia and the acidosis. Hyperkalemia by itself, rather than hypoaldosteronism per se, caused the acidosis in this patient. Hyperkalemia apparently suppresses urinary ammonium excretion and thus interferes with urinary acidification.

No abstract

A 69-year-old woman presented with persistent dyspnea and continuous coughing and mediastinal mass. The mass was found to be a malignant thymoma and was resected incompletely. A full-blown nephrotic syndrome appeared 1 year after removal of the thymoma. Renal biopsy revealed minimal-change glomerulonephritis. There was no evidence of other autoimmune diseases or causes of the minimal-change glomerulonephritis.

1) we have demonstrated the independence of insulin action on glucose and potassium uptake in vivo, 2) we documented the existence of selective insulin resistance in the above patients, 3) we speculate, that in patients with a normal response to insulin on one parameter of its actions, and subnormal response on another parameter, a postreceptor defect rather than a receptor abnormality must exist.

Complete bilateral malignant ureteral occlusion was relieved by introduction of a nephrostomy tube, first into the right kidney and 3 weeks later into the left kidney. When the second nephrostomy tube was introduced, the right kidney had recovered sufficiently to eliminate the uremic environment and to serve as control organ. This offered the rare opportunity to study in man the function of the kidney following chronic obstruction, independent of systemic influences on tubular function, such as uremia, secondary hyperparathyroidism and the state of hydration of the patient. In the left (‘experimental’) kidney glomerular filtration (GFR) was markedly reduced and fractional and, on occasions, absolute excretion of sodium, calcium and magnesium exceeded simultaneous values in the right (‘control’) kidney. During hypotonic saline and mannitol diuresis, free water clearance relative to GFR and calculated distal delivery of sodium in the experimental kidney exceeded control values by more than twofold and more than threefold, respectively. Distal tubular function, as judged by the ability to generate free water and exchange sodium for potassium, appeared spared. These data suggest that in obstructive uropathy in man there is an intrarenal resetting of the glomerulotubular balance resulting in diminution of proximal tubular reabsorption of sodium, water and probably also divalent cations, which leads to enhanced tubular flow (‘overperfusion’) in the relatively intact distal nephrons. This change in glomerulotubular balance is brought about by an undefined mechanism, initiated by ureteral occlusion or by reduction in nephron population or their combination, and contributes to the profuse natriuresis and diuresis seen following the relief of ureteral occlusion.