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Biomedical subjects

R H Sterns

Publications and source records attributed to R H Sterns.

At least 37 records · Page 2Linked to original sources
PubMed1989

Brain dehydration and neurologic deterioration after rapid correction of hyponatremia.

We made rats severely hyponatremic, varying the rate of onset and duration of the disturbance, and then compared rapid correction to slow correction. An acute fall in the plasma Na to 106 mEq/liter within seven hours caused seizures and coma, but these findings resolved and survival was 100% after either rapid or slow correction. A more gradual fall in plasma Na to 95 mEq/liter in three days caused neither seizures nor coma. Measurements of brain water and electrolytes showed that adaptive losses of brain Na and K (maximally depleted within seven hours) and slower losses of non-electrolyte solutes progressively reduced brain edema. After three days of hyponatremia, rapid correction to 119 mEq/liter with 1 M NaCl or to 129 mEq/liter by withdrawing DDAVP caused brain dehydration because lost brain K and non-electrolyte solutes were recovered slowly. This treatment was followed by a delayed onset of severe neurologic findings, demyelinating brain lesions and a mortality rate of over 40%. Slow correction (0.3 mEq/liter/hr) avoided these complications and permitted 100% survival. We conclude that the rat adapts quickly to hyponatremia and can survive with extremely low plasma sodium concentrations for prolonged periods. Although rapid correction is well tolerated when hyponatremia is of brief duration, it may cause brain damage in animals that have had time to more fully adapt to the disturbance.

Animals↗
PubMed1989

Extrarenal potassium adaptation: the role of aldosterone.

1. Prior adaptation to a high potassium (HK) diet reduces the increment in plasma potassium after nephrectomy and acute potassium loading. Previous work has suggested that this 'extrarenal potassium adaptation' is due to direct stimulation of cellular potassium uptake by chronic hyperaldosteronism. 2. In contrast, we have shown that when dietary potassium is withdrawn from HK rats, large urinary potassium losses persist, resulting in 'paradoxical potassium depletion'. This potassium depletion facilitates cellular potassium uptake and is, at least in part, responsible for extrarenal potassium adaptation. 3. To try to reconcile these observations, we explored further the role of aldosterone in extrarenal potassium adaptation. When dietary potassium was withdrawn from chronically adrenalectomized HK rats, paradoxical potassium depletion was markedly blunted and extrarenal potassium adaptation could not be demonstrated. Similarly, urinary potassium losses and potassium depletion were reduced when acute adrenalectomy was performed concomitantly with dietary potassium withdrawal. 4. We were unable to confirm previous studies showing extrarenal potassium adaptation in the absence of potassium depletion. Thus, extrarenal potassium adaptation did not occur after pretreatment with chronic high-dose mineralocorticoid, after prior adaptation to a sodium-free diet, or after prior adaptation to an extremely HK diet in the absence of dietary potassium withdrawal. 5. We conclude that chronic hyperaldosteronism is important in extrarenal potassium adaptation, but probably not via direct enhancement of cellular potassium uptake. Rather, in HK animals, hyperaldosteronism magnifies urinary potassium losses during fasting and thus promotes potassium depletion, which in turn facilitates the uptake of an acute potassium load.

Adaptation, Physiological↗
PubMed1987

Acute idiopathic tubulointerstitial nephritis: report of two cases and review of the literature.

Two patients who presented with severe renal failure and evidence of generalized proximal tubular dysfunction were found to have severe diffuse acute tubulointerstitial nephritis on renal biopsy. No etiology could be found in either case. Both patients had dramatic improvement in renal function following steroid therapy. In the first reported case of its kind, one patient relapsed when steroids were withdrawn, but improved again with reinstitution of steroid therapy. These cases, as well as others in the literature, show that steroids are effective and may be necessary to improve renal function in some patients with acute idiopathic tubulointerstitial nephritis. Evidence of proximal tubular dysfunction is a clue to the presence of this disorder.

Acute Disease↗
PubMed1987

Severe symptomatic hyponatremia: treatment and outcome. A study of 64 cases.

A serum sodium concentration of 110 mmol/L or less is thought to be extremely dangerous; mortality rates of 33% to 86% have been cited. Experience at the University of Rochester School of Medicine does not corroborate this widespread belief. Among 62 patients with 64 episodes of severe hyponatremia, the mortality rate was only 8%, and most deaths were caused by underlying diseases; with a serum sodium concentration of 105 mmol/L or less, the mortality rate was 5%. Rapid correction of hyponatremia did not account for this favorable prognosis. Only 6% of the 64 cases were corrected to a serum sodium concentration of 120 mmol/L at recommended rates of 1.5 to 2 mmol/(L.h); half of the patients achieved this rate of correction because of a spontaneous water diuresis. In some settings, vigorous therapeutic efforts may have contributed to an adverse outcome. Rapid correction of hyponatremia is not indicated just because the serum sodium concentration is extremely low.

Acute Disease↗
PubMed1986

Osmotic demyelination syndrome following correction of hyponatremia.

The treatment of hyponatremia is controversial: some authorities have cautioned that rapid correction causes central pontine myelinolysis, and others warn that severe hyponatremia has a high mortality rate unless it is corrected rapidly. Eight patients treated over a five-year period at our two institutions had a neurologic syndrome with clinical or pathological findings typical of central pontine myelinolysis, which developed after the patients presented with severe hyponatremia. Each patient's condition worsened after relatively rapid correction of hyponatremia (greater than 12 mmol of sodium per liter per day)--a phenomenon that we have called the osmotic demyelination syndrome. Five of the patients were treated at one hospital, and accounted for all the neurologic complications recorded among 60 patients with serum sodium concentrations below 116 mmol per liter; no patient in whom the sodium level was raised by less than 12 mmol per liter per day had any neurologic sequelae. Reviewing published reports on patients with very severe hyponatremia (serum sodium less than 106 mmol per liter) revealed that neurologic sequelae were associated with correction of hyponatremia by more than 12 mmol per liter per day; when correction proceeded more slowly, patients had uneventful recoveries. We suggest that the osmotic demyelination syndrome is a preventable complication of overly rapid correction of chronic hyponatremia.

Adult↗
PubMed1986

Paradoxical potassium depletion: a renal mechanism for extrarenal potassium adaptation.

Following nephrectomy and acute potassium loading, animals previously maintained on a high potassium diet have a smaller increment in plasma potassium than do animals on a control diet. The mechanism of this "extrarenal potassium adaptation" is not known. To explore the role of potassium depletion in this process, we studied rats adapted to either a high potassium (HK) or control (C) diet. When dietary potassium was withdrawn, urinary potassium losses in HK rats greatly exceeded those in C rats for at least two days, leading to greater potassium depletion in HK than C animals. A smaller increment in plasma potassium in HK compared to C rats was seen only after prolonged fasting preceded nephrectomy and acute potassium loading. Correction of potassium depletion incurred during fasting abolished extrarenal potassium adaptation. We conclude: after withdrawal of dietary potassium, urinary potassium losses are much greater in HK than in C rats; if the duration of dietary potassium deprivation is sufficient, these urinary potassium losses will cause potassium-adapted animals to paradoxically become more potassium depleted than controls; and this paradoxical potassium depletion may be responsible for extrarenal potassium adaptation.

Adaptation, Physiological↗
PubMed1985

'Page kidney'. Hypertension caused by chronic subcapsular hematoma.

Conditions analogous to an experimental model of hypertension described by Page in 1939 are called "Page kidney." In chronic subcapsular hematoma, the most common clinical counterpart to Page's model of renal parenchymal compression, a review of the literature reveals that hypertension is usually cured by nephrectomy, but is seldom cured by mere evacuation of the hematoma. To our knowledge, no patient remaining hypertensive after evacuation has undergone nephrectomy. In the patient described herein, a liquified subcapsular hematoma reaccumulated after it was drained percutaneously, and therefore it had to be evacuated surgically. Persistent renin-mediated hypertension, however, prompted curative nephrectomy. The response to more prolonged percutaneous drainage might have guided more effective initial surgery.

Adolescent↗
PubMed1985

Postpartum renal vein thrombosis.

Renal vein thrombosis in adults is usually a complication of the nephrotic syndrome. Rarely, it has been reported in nonnephrotic women postpartum. The thrombosis may be a complication of the hypercoagulable state associated with both the nephrotic syndrome and pregnancy. Two postpartum patients with renal vein thrombosis and no prior history of renal disease are reported here. Neither patient had heavy proteinuria. In both cases, pyelonephritis was suspected clinically and the diagnosis of renal vein thrombosis was first suggested and confirmed by radiologic examination. Renal vein thrombosis should be considered in women presenting postpartum with flank pain.

Angiography↗
PubMed1985

Potassium supplementation via the dialysate in continuous ambulatory peritoneal dialysis.

A small percentage of patients treated with continuous ambulatory peritoneal dialysis (CAPD) may become hypokalemic. Since both the intravenous and oral routes for potassium repletion have disadvantages, we studied the feasibility, effectiveness, and safety of acute potassium loading via the dialysate in patients on CAPD. Five patients were studied during an exchange containing 20 mEq/L of potassium. This was well tolerated and led to a gradual increase in the plasma potassium concentration (.44 +/- .11 mEq/L) as about three-fourths of the intraperitoneal load was absorbed, most of it by two hours. The greatest increase in the plasma potassium concentration was .63 mEq/L. A separate patient developed intense abdominal pain during an exchange containing 40 mEq/L of potassium. We conclude that the dialysate is a safe and effective route for acute potassium repletion during CAPD when the dialysate potassium concentration does not exceed 20 mEq/L.

Abdomen↗
PubMed1984

Renal infarction due to renal artery dysplasia with dissection. Report of a case in a normotensive patient.

A previously healthy 44-year-old man with well-documented normotension had a sudden onset of left flank pain and delayed onset of constitutional symptoms, hematuria, and elevations of lactic dehydrogenase, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, and creatinine levels. Angiography revealed unilateral renal artery fibromuscular dysplasia with dissection and infarction. In the year since, he has remained well and normotensive without therapy. The literature is reviewed.

Adult↗