Biomedical subjects
Publications and source records attributed to P Szylman.
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.
This study was designed to evaluate the mechanisms of adaptation to chronic potassium loading after bilateral adrenalectomy. Studies were performed in Sprague-Dawley rats subjected to 3 days of normal diet and 9 days of high KCl diet followed by adrenalectomy or sham operation on the thirteenth day and 9 additional days of potassium loading (groups 1 and 2, respectively). Animals that underwent adrenalectomy and intact animals, both receiving a normal diet, served as the control groups (groups 3 and 4, respectively). Plasma potassium, urinary potassium and sodium excretion rates, plasma aldosterone and insulin, and Na+-K+ ATPase activity in renal cortical and medullary homogenates were measured. Within 5 days of adrenalectomy the urinary potassium excretion rate in potassium-loaded rats that underwent adrenalectomy (group 1) reached the level observed in potassium-loaded intact rats (group 2), but a significant elevation in plasma potassium levels among rats in group 1 was noticed. In both of the potassium-loaded groups plasma insulin levels and renal cortical and medullary Na+-K+ ATPase activity were significantly higher compared with those in respective control groups receiving a normal diet. Acute clearance experiments carried out in adrenalectomized rats infusing the sera of the potassium-adapted rats that underwent adrenalectomy (obtained at the end of the chronic experiment) showed an uprise in urinary potassium excretion. This result was not observed after the infusion of control sera. These findings suggest that full renal adaptation to chronic potassium loading can be achieved in the absence of aldosterone through mechanisms that might be related to elevated plasma insulin levels (extrarenal); also, a humoral factor associated with the renal adaptation cannot be ruled out.
An outbreak of organic mercurial intoxication in a peasant family from the Jordan West Bank is reported. Extrapyramidal symptoms, muscular wasting, oral ulcerations, and renal tubular dysfunction were the main manifestations. Hpyokalemia (1.9-2.7 mEq/l) due to urinary potassium wasting was present in all 4 patients. Type II RTA was observed in 2 cases. Urinary ammonium excretion was increased over the range predicted by the given urinary pH in all the patients. Intrinsic tubular damage, nonreabsorbable anions of catabolic origin, increased prostaglandin synthesis inducing renin-angiotensin axis activation, and, consequently, inappropriate relatively high levels of aldosterone, are advanced as an explanation for potassium wasting.
Pregnancy is an unusual event in patients with chronic renal failure undergoing dialysis. The outcome in these cases is usually poor. We report a pregnancy complicated by severe renal insufficiency that was managed successfully by continuous ambulatory peritoneal dialysis. Dialysis was initiated at 24 weeks' gestation. At 34 weeks, premature labor associated with peritonitis resulted in the spontaneous delivery of a healthy male infant weighing 2400 g. The use of continuous ambulatory peritoneal dialysis during pregnancy offers theoretical advantages compared with hemodialysis. Our case, added to the available limited experience with this new modality, suggests that it may be an appropriate approach in women developing renal disease for the first time during pregnancy.
UNLABELLED: The effects of insulin on in vivo glucose use and potassium uptake in healthy humans are well documented. However, the interrelationship between these two processes is not fully defined. In order to characterize it, we have used the euglycemic clamp technique on six normal volunteers, two patients with acanthosis nigricans and insulin resistance (AN), and one patient with idiopathic nonazotemic hyperkalemia (HK). In the basal state, all patients had normal fasting blood sugar, the AN patients had fasting hyperinsulinemia (600% of controls), and the HK patient had an elevated plasma potassium level of 5.1 mmol/L (n = 4.2 +/- 0.2 mmol/L). During low dose (1 mU/kg.min), and high dose (10 mU/kg.min) insulin infusions, normals used glucose at a rate of 220 +/- 10 and 470 +/- 20 mg/M2.min, respectively. The HK patient had a normal glucose use at both infusion rates, but the AN patients had a 20% decrease of glucose use compared to normals at the two infusion rates. In normal patients, plasma potassium fell by 0.7 and 1.4 mmol/L at the end of the two infusion periods, respectively. AN patients had a similar fall in potassium, but the HK patient displayed no change in plasma potassium levels during a low dose insulin infusion, and only a 0.6 mmol/L drop during the high dose insulin infusion. These results indicate that: 1) patients with AN are resistant to insulin action on glucose use, 2) AN patients have a normal response to insulin on potassium uptake, 3) HK is a patient with normal response to insulin on glucose use, and 4) this patient is resistant to insulin action on potassium uptake. IN CONCLUSION: 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.
We report a hypertensive patient with nonazotemic hyperkalemia caused by a combined disturbance in both the internal and external balance of potassium. During a follow-up of 30 months, exacerbations of hyperkalemia were observed, interposed with a return to the previous baseline. Two brief normokalemic periods were recorded. Blood pressure tended to be higher during hyperkalemic peaks. The following findings were detected: (1) hyperchloremic hyperkalemic acidosis with normal glomerular filtration rate, adequately elevated plasma aldosterone levels, and normovolemia; (2) a tubular defect in potassium excretion, refractory to intravenous sodium sulfate (nonreabsorbable anion) and mineralocorticoids; (3) impaired tissue uptake of potassium under insulin administration; (4) exaggerated hyperkalemia following beta-adrenergic blockade and blunted hypokalemic response to a beta-agonist; and (5) a defect in Na/K transport in erythrocytes detected in vitro, coexistent with an elevated level of free digoxin-like immunoreactive factor in serum. These results suggest that our patient had a generalized abnormality in potassium transport.
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Renal tubular function, with special emphasis on potassium excretion, was studied in three patients with medullary sponge kidney (MSK). Urinary acidification and concentration abilities were impaired, while glomerular filtration rates remained normal. After short-term intravenous (IV) potassium chloride loading, maximal excretion of potassium was lower in the patients with MSK than in the normal controls. The kaliuretic response to IV sodium sulfate and acetazolamide infusion was maintained. The capacity of the kidney to sustain potassium balance under conditions of either long-term potassium loading or depletion was preserved. We have concluded that the medullary and papillary segments of the human collecting duct, have an important role in the handling of short-term potassium loading. The integrity of these segments, however, is not essential for adaptation to prolonged potassium surfeit or dietary depletion.
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Tubular handling of sodium and phosphate were studied in 4 patients with cirrhosis and ascites. The control group consisted of 5 patients with cirrhosis without sodium retention. The degree of phosphaturia was assumed to reflect proximal tubular reabsorption. Whereas fractional excretion of phosphate was comparable in both groups, fractional excretion of sodium was strikingly diminished in the patients with ascites. This observation suggests that sodium retention in these patients occurs beyond the proximal tubule. This interpretation is in accord with our previous observation, based on clearance data, that the proximal tubular reabsorption of sodium in cirrhosis may be normal even in the face of edema formation.
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.
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