Robert S. Swenson

The Nephrotic Syndrome: A Complication of Massive Obesity

Abstract Four patients with massive obesity and the nephrotic syndrome were studied. Congestive heart failure was not clinically apparent, and measured cardiac output was elevated; however, right a...

Acquired cystic disease of the end-stage kidney

The development of multiple cysts in the previously noncystic chronically diseased kidneys of patients undergoing long-term dialysis appears to be associated with spontaneous renal bleeding and benign and malignant renal tumors. Two cases of acquired cystic disease with renal hemorrhage and adenocarcinoma are presented; metastases occurred in one patient and the other had bilateral carcinoma requiring bilateral nephrectomy. Combined data from 13 studies indicate acquired cystic disease occurs in one third of patients undergoing maintenance hemodialysis and is associated with adenocarcinoma in 4 percent of cases. Four cases of metastases and five deaths linked to acquired cystic disease have been reported. Eight of 24 patients with acquired cystic disease and clinical manifestations of renal bleeding had renal adenocarcinoma. Autopsy series indicate tumors associated with acquired cystic disease are usually benign but commonly bilateral and multiple. Cystic transformation of the end-stage kidney is more frequent after several years of hemodialysis. It is suggested that patients receiving dialysis treatments for more than three years have a baseline radiologic examination of the kidneys so that subsequent problems can be more easily identified and evaluated.

Evidence that parathyroid hormone is not required for phosphate homeostasis in renal failure

Varying degrees of renal failure were produced by surgical reduction of renal mass in normal dogs and in thyroparathyroidectomized dogs (TPTX) in whom serum calcium levels were maintained in the normal range by the administration of vitamin D. Both groups of dogs maintained normal serum phosphate levels in spite of progressive decreases in glomerular filtration rates (GFR). Furthermore, both groups of dogs were able to increase the fractional excretion of phosphate as GFR decreased. Thus the same renal response to loss of GFR was maintained in the complete absence of parathyroid tissue. Finally, stable serum phosphate levels and increased fractional excretion of phosphate in response to a decrease in GFR were also demonstrated in acutely TPTX dogs who were not receiving vitamin D. These results indicate that phosphate homeostasis can be maintained in renal failure in the total absence of parathyroid hormone secretion.

Acquired renal cystic disease and renal neoplasms in hemodialysis patients

Noninvasive imaging studies were performed on 26 patients undergoing chronic hemodialysis. We found cysts in 46% of patients and neoplasms in 7.7%. The cysts were relatively easy to detect. However, the neoplasms were very difficult to detect; this problem has been described before in the literature. The natural history of acquired cystic disease and neoplasms in hemodialysis patients is largely unknown. A review of the problems associated with the imaging and management of these patients is included.

Evidence that hemodialysis does not improve the glucose tolerance of patients with chronic renal failure

Abstract Oral glucose tolerance tests were performed in 16 patients with chronic renal failure undergoing hemodialysis. In ten patients, studies were performed before and after one dialysis, while six patients were studied immediately prior to the start of chronic hemodialysis and just after the fifteenth dialysis. Hemodialysis did not lead to improvement in either the plasma glucose or growth hormone response to the oral glucose challenge. There was, however, a modest increase noted in the plasma insulin level 2 hr after the oral glucose challenge following dialysis. On the other hand, there was not any change in the overall relationship between the plasma glucose and insulin response to the oral glucose load as a result of dialysis. These results indicate that chronic hemodialysis as it is routinely conducted in the treatment of patients with chronic renal failure has, at best, a relatively modest effect on the plasma glucose, growth hormone, and insulin responses to an oral glucose challenge.

Cardiac arrest due to oral potassium administration

Cardiac arrest developed in two patients after the administration of oral potassium. Neither patient had renal insufficiency, but both had underlying heart disease. In one patient fatal ventricular fibrillation developed 4 days after he received an aortic valve replacement for aortic stenosis and while he was receiving oral potassium supplements. The serum potassium level before cardiac arrest was 8.1 meq. The second patient had angina and was given 40 meq of potassium orally 15 minutes after an exercise test which produced chest pain and S-T segment depression. One hour later, ventricular fibrillation developed. Resuscitation was successful. Both patients had electrocardiographic evidence of hyperkalemia. Oral administration of potassium may produce severe cardiac toxicity in patients with heart disease even when renal function is clinically normal.

Comparison of the Effects of Metabolic Acidosis and Acute Uremia on Carbohydrate Tolerance

In an attempt to assess the role of metabolic acidosis in the glucose intolerance of uremia, we have estimated insulinmediated glucose uptake in normal dogs, in acidotic dogs with normal renal function, and in uremic dogs. Mean steady state plasma glucose and insulin levels were measured in eighteen dogs (pH 7.4 ± .01) during constant infusion of glucose and insulin, while endogenous insulin secretion was suppressed by infusion of propranolol and epinephrine. The dogs were then divided into three groups: moderate acidosis was produced by giving 7 gm. NH4Cl/ day for four days; severe acidosis, 12 gm. NH4Cl/day for four days; and uremia (serum creatinine 15.7 ± 0.2 mg. per cent) by anastomosing both ureters to the vena cava. Duplicate infusions were then performed and the results compared to control values. Plasma insulin levels were identical, despite the presence of either acidosis or uremia. The mean increase in plasma glucose in moderate acidosis (pH 7.2 ± 0.1) over controls was 39 mg./l00 ml. (p < .05); in severe acidosis (pH 7.0 ± .04) plasma glucose increased by 69 mg,/100 ml. (p < .01). However, the mean increase in plasma glucose (149 mg./100 ml.) in uremia (pH 7.3 ± .03) was significantly greater (p < .005) than that following acidosis, although the pH did not significantly fall. Thus, although metabolic acidosis results in deterioration of glucose tolerance, the magnitude of the change does not seem able to account for the carbohydrate intolerance of uremia.

A Paradoxical Effect of Chlorpropamide on the Plasma Glucose and Immunoreactive Insulin Response to Intravenous Glucose in Normal Dogs

The effect of various doses of chlorpropamide on plasma glucose and immunoreactive insulin responses to an acute intravenous glucose challenge has been studied in normal dogs. The effects of chlorpropamide were compared to those of placebo in each dog. The administration of 375 mg. of chlorpropamide for four days decreased the ability of the dogs to dispose of a glucose load, and the deterioration in glucose tolerance was accompanied by a marked suppression of the plasma insulin response. Administration of 125 mg. of chlorpropamide for four days led to changes that were qualitatively similar but quantitatively less striking. These results indicate that excessive amounts of chlorpropamide can lead to deterioration in glucose tolerance; this effect seems analogous to induction of glucose intolerance in normal subjects by administration of insulin, as first described by Somogyi. When the chlorpropamide was decreased to a daily dose of 50 mg., dogs were able to dispose of the intravenous glucose load more efficiently than normal. However, this improvement in glucose tolerance was not associated with a significant rise in plasma insulin response. Thus, although it seems reasonable to attribute deterioration in glucose tolerance after excessive doses of chlorpropamide at least partly to inhibition of insulin release, the improvement that occurs after smaller doses does not appear to be due to an absolute increment in the plasma insulin response to glucose.