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Biomedical subjects

M R Rudnick

Publications and source records attributed to M R Rudnick.

29 records · Page 2Linked to original sources
PubMed1984

Thrombotic microangiopathy and renal failure associated with antineoplastic chemotherapy.

Five patients with carcinoma developed thrombotic microangiopathy (characterized by renal insufficiency, microangiopathic hemolytic anemia, and usually thrombocytopenia) after treatment with cisplatin, bleomycin, and a vinca alkaloid. One patient had thrombotic thrombocytopenic purpura, three the hemolytic-uremic syndrome, and one an apparent forme fruste of one of these disorders. Histologic examination of the renal tissue showed evidence of intravascular coagulation, primarily affecting the small arteries, arterioles, and glomeruli. Because each patient was tumor-free or had only a small tumor at the onset of this syndrome, the thrombotic microangiopathy may have been induced by chemotherapy. Diagnosis of this potentially fatal complication may be delayed or missed if renal tissue or the peripheral blood smear is not examined, because renal failure may be ascribed to cisplatin nephrotoxicity and the anemia and thrombocytopenia to drug-induced bone marrow suppression.

Adult↗
PubMed1982

Correction of drug binding defects in uremia in vitro by anion exchange resin treatment.

Serum protein binding of weakly acidic drugs is impaired in uremia, but that of basic drugs tends to be normal. Treatment of uremic serum with anion exchange resin (Amberlite CG-400, acetate form) corrected binding defects for three acidic drugs (nafcillin, salicylate and sulfamethoxazole) but did not affect the binding of two basic drugs (trimethoprim and quinidine). Resin treatment of normal human serum did not alter the binding of these five drugs. Extraction of the acetate buffer eluate from resin exposed to uremic serum with n-butyl chloride at acidic pH (3.0) resulted in a fraction that could induce similar binding defects in normal human serum. The factor(s) responsible for binding defects in uremia appears to be lipid soluble, weakly acidic, and dialyzable. It is believed to be tightly bound to albumin at physiologic pH, but dissociates from it at acidic pH. These findings further support the previously proposed hypothesis that drug-binding defects in uremia are due to accumulation of certain endogenous metabolic product(s).

Adult↗
PubMed1982

Diagnostic strategies in disorders of fluid, electrolyte and acid-base homeostasis.

Our understanding of the physiology and biochemistry of acid-base and fluid-electrolyte regulations has greatly expanded in recent years. Key physiologic principles have emerged that now permit rational diagnosis and therapy of clinical disorders of serum electrolyte concentration. This paper describes diagnostic strategies based upon these principles. The etiology of the myriad factors in hyponatremia is best derived by first measuring serum tonicity and then assessing extracellular fluid volume. The hyper-, iso- and hypotonic hyponatremia are defined, and the hypotonic group is subclassified into hypo-, iso- and hyper volemic forms. The hypernatremias are best categorized by their state of volume expansion. Classification into the hypo-, hyper- and isovolemic hypernatremias simplifies their diagnosis. Metabolic acidoses are classified in terms of the anion gap. Clinical and chemical aspects of increased and normal anion gap acidoses are described. Metabolic alkaloses require a source of new bicarbonate and its retention by the kidney. The means by which new alkali is synthesized and urinary loss prevented serve to effectively classify the alkaloses. Hypokalemic syndromes are defined in terms of associated changes in body potassium. The potassium-depleted states are further subclassified by whether normotension or hypertension is associated. Hyperkalemia is produced by redistribution of cellular and extracellular potassium or by increased body potassium. Defects in the renin-angiotensin-aldosterone-distal renal tubule effector arm usually underlie hyperkalemic states, which are than classified in terms of this regulatory hormonal cascade. Classifications for disordered serum concentrations of calcium, magnesium, phosphorus and uric acid are presented. Hormonal, metabolic and renal regulatory factors form the basis for an organized approach to these disorders.

Acid-Base Imbalance↗
PubMed1981

Partial purification and characterization of the drug-binding-defect inducer in uremia.

The chemical basis of drug-binding defects in uremia was investigated by studying the effects of extraction of uremic sera with an organic solvent (n-butyl chloride). Extraction of uremic sera at acidic pH (3.0) with n-Butyl chloride fully corrected the binding defects for three acidic drugs (nafcillin, sulfamethoxazole, and salicylate), whereas binding of two basic drugs (trimethoprim and quinidine) was unaffected by similar treatment. When added to normal human serum or purified human serum albumin, the organic solvent layer was capable of inducing binding defects similar to those seen in uremia. Further fractionation of the organic solvent layer with purified human serum albumin at physiologic pH (7.4), followed by reacidification and extraction of the acidified albumin layer with the same solvent, gave a homogeneous fraction on thin-layer chromatography. This homogeneous fraction could induce the binding defects observed in uremia when added to normal human sera. This factor(s) is apparently a dialyzable and weakly acidic compound. It is lipid-soluble and tightly bound to albumin at physiologic pH, but extractable at acidic pH. Its molecular weight is approximately 500 or less. These findings strongly support the hypothesis that the drug-binding defect in uremia is due to accumulation of endogenous metabolic products rather than to an intrinsic structural abnormality in serum albumin.

Biological Products↗
PubMed1980

The kidney in health and disease: XVIII: lactic acidosis and the elevated anion gap (II).

This concluding article of a two-part discussion deals with clinical presentations and management of the basic types of lactic acidosis - with and without appaent hypoxia - and the various complicating conditions that may coexist with them. Although symptomatic treatment is essential, cure can be effected only by seeking and treating the underlying cause of the electrolyte derangement.

Acidosis↗
PubMed1980

Effects of placebo versus guanabenz on hypertensive out-patients.

The objectives of this study were two-fold: (1) 1 4-week multicentre, randomized, double-blind efficacy comparison of placebo and guanabenz acetate, a new centrally acting antihypertensive drug, in 168 hypertensive out-patients and (2) a more accurate determination of the incidence of drug-related, non-specific side-effects. Both treatment groups were comparable: 68% female, 63% black, mean age 53 years; 57% mild, 32% moderate, 11% moderately severe hypertensives. Seventy-six placebo patients completed 4 weeks and had a mean supine diastolic blood pressure (SDBP) decrease from 105 to 101 mm Hg (p < 0.01). Seventy-nine guanabenz patients completing 4 weeks had a mean SDBP decrease from 104 to 92 mm Hg (p < 0.01). All of the placebo responses and 10/12 mm Hg of the guanabenz response occurred during Week 1. Clinically significant individual SDBP decreases occurred in thirty-one (41%) placebo and fifty-five (70%) guanabenz-treated patients (p < 0.01). Mean daily guanabenz dose was 24 mg. Drug-related biochemical or electrocardiographic abnormalities were absent. Side-effects of sedation and dry mouth were recorded two and three times more frequently, respectively, in guanabenz as compared to placebo patients. Side-effects usually occurred within Week 1 and diminished in incidence thereafter. Consequently, in these patients it appeared that: (1) guanabenz was an effective, well-tolerated drug, (2) placebo effects on efficacy were significant, occurred early and remained stable, and (3) placebo and guanabenz side-effects were mainly sedation and dry mouth.

Adult↗
PubMed1980

Human pancreatic polypeptide in chronic renal failure and cirrhosis of the liver: role of kidneys and liver in pancreatic polypeptide metabolism.

Basal plasma concentrations of human pancreatic polypeptide (PP) were measured in 14 patients with chronic renal failure (CRF), 13 patients with cirrhosis of the liver, and age-matched controls. PP was significantly higher in patients with CRF than in controls (817 +/- 183 vs. 157 +/- 118 pg/ml; P < 0.005). The degree of PP elevation in patients with CRF correlated well with the degree of their renal insufficiency (r = 0.85; P < 0.001). Fractionation of plasma over Sephadex G-50 columns revealed comparable elution patterns in patients with CRF and in normal controls. Hemodialysis had no effect on the PP concentration. We also determined arterial venous PP concentration differences and plasma blood flow across the kidneys and liver in 13 patients with cirrhosis and arteriovenous differences across of the liver in 13 controls with normal hepatic and renal functions. The mean PP concentration was significantly higher in arterial plasma than in renal venous plasma (143 +/- 24 vs. 123 +/- 23 pg/ml; P < 0.025). Renal fractional extraction was 17.2 +/- 6.6%, and renal clearance of PP was 151 +/- 47 ml/min. No significant extraction of PP occurred across the liver. It is concluded that the kidneys, but not the liver, are important sites for the metabolism of PP and that elevated PP concentrations in patients with CRF may contribute to their uremic syndrome.

Adult↗
PubMed1979

Acute massive hydrothorax complicating peritoneal dialysis, report of 2 cases and a review of the literature.

Acute massive right-sided hydrothorax is a relatively rare but serious complication of peritoneal dialysis and may be responsible for the development of dyspnea during peritoneal dialysis. The pleural fluid appears to arise from the peritoneal dialyzate based on the time of its appearance and its chemical composition. It should be included in the differential diagnosis when a patient becomes dyspneic during peritoneal dialysis along with exaccerbation of congestive heart failure, pneumonia, atelectasis, and purulent bronchitis. Its occurrence is an indication to stop the peritoneal dialysis and contraindicates further use of this form of dialysis. Treatment may be conservative or aggressive (thoracentesis) depending on the clinical condition of the patient. Etiology is poorly understood. In some cases, there may be traumatic diaphragmatic fenestrations, but the majority of cases appear to be due to less well defined communications between the peritoneal and pleural spaces.

Dyspnea↗