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M A Perazella

Publications and source records attributed to M A Perazella.

64 records · Page 4Linked to original sources
PubMed1994

Nephrotic syndrome associated with agnogenic myeloid metaplasia.

Agnogenic myeloid metaplasia (AMM), a myeloproliferative disorder of clonal origin, can affect the kidneys via several mechanisms. Associated disorders include asymptomatic interstitial extramedullary hematopoiesis, obstructive uropathy and nephrolithiasis. Currently, there are no descriptions of the nephrotic syndrome associated with AMM. We present a case of AMM associated with the nephrotic syndrome, a mesangial proliferative glomerular lesion and extramedullary hematopoiesis.

Aged↗
PubMed1993

Renal mechanism of trimethoprim-induced hyperkalemia.

OBJECTIVES: 1) To determine the incidence and severity of hyperkalemia during trimethoprim therapy. 2) To test the hypothesis that trimethoprim inhibits renal potassium excretion by blocking sodium channels in the mammalian distal nephron. PATIENTS: Thirty consecutive patients who were treated with trimethoprim-containing drugs. All patients included in the study had the acquired immunodeficiency syndrome (AIDS). EXPERIMENTAL ANIMALS: Thirty-nine male Sprague-Dawley rats receiving normal rat chow and tap water (allowed free access). INTERVENTION: Humans: high dose (20 mg/kg per day) of trimethoprim therapy. Rats: trimethoprim (9.6 mg/h per kg body weight) was infused intravenously or into the renal distal tubules (1 mmol/L). MEASUREMENTS: Humans: Serum and urine electrolyte levels, serum creatinine, renin, aldosterone, and cortisol levels were measured, and the transtubular potassium gradient was calculated. Rats: The effects of trimethoprim infusion on urinary sodium, chloride, and potassium concentration and urine volume were measured. Sodium, chloride, potassium, and inulin concentrations were measured in fluid samples obtained from kidney distal tubules. The voltage across the wall of the distal tubule was measured. RESULTS: Humans: Trimethoprim increased the serum potassium concentration by 0.6 mmol/L (95% Cl, 0.29 to 0.95 mmol/L) despite normal adrenocortical function and glomerular filtration rate. Serum potassium levels greater than 5 mmol/L were observed during trimethoprim treatment in 15 of 30 patients. Rats: Intravenous trimethoprim inhibited renal potassium excretion by 40% (Cl, 21% to 60%) and increased renal sodium excretion by 46% (Cl, 9% to 83%). Trimethoprim (1 mmol/L) in tubule fluid inhibited distal tubule potassium secretion by 59% (Cl, 26% to 92%) and depolarized the lumen-negative transepithelial voltage by 66% (Cl, 46% to 85%). CONCLUSIONS: Trimethoprim (an organic cation) acts like amiloride and blocks apical membrane sodium channels in the mammalian distal nephron. As a consequence, the transepithelial voltage is reduced and potassium secretion is inhibited. Decreased renal potassium excretion secondary to these direct effects on kidney tubules leads to hyperkalemia in a substantial number of patients being treated with trimethoprim-containing drugs.

AIDS-Related Opportunistic Infections↗
PubMed1993

Renal failure and severe hypokalemia associated with acute myelomonocytic leukemia.

The leukemias have long been associated, albeit rarely, with the development of renal failure and several metabolic perturbations. While renal insufficiency may result from a variety of mechanisms in the setting of leukemia, severe leukostasis with microvascular insufficiency and renal parenchymal infiltration by blast cells are rare and infrequently described etiologies. In addition, hypokalemia can occur from lysozyme-induced renal tubular injury with inappropriate kaliuresis. We present a case of acute myelomonocytic leukemia that was complicated by renal failure and severe hypokalemia and discuss the probable mechanisms.

Aged↗
PubMed1993

Successful treatment of cystinuria with captopril.

Cystinuria is an autosomal recessive hereditary disorder associated with nephrolithiasis and its attendant complications. Traditional management aimed at increasing urinary cystine solubility using oral alkali, D-penicillamine, or mercaptopropionyglycine is often unsuccessful due to intolerable side effects. Two cystinuric patients intolerant of traditional therapy were treated with captopril for 1 year, resulting in a marked decline in urinary cystine excretion. Neither patient experienced recurrent nephrolithiasis or adverse drug effects. Captopril should be considered an alternative to traditional drug management of cystinuria.

Adult↗
PubMed1993

NSAID nephrotoxicity revisited: acute renal failure due to parenteral ketorolac.

The success of ketorolac as a nonnarcotic analgesic is likely to propagate its widespread use to control moderate to severe postoperative pain. Indeed, of the patients treated with ketorolac and described in the medical literature, nearly 90% had had a major surgical procedure. Since any such procedure may be associated with significant third-spacing of the fluid and result in renal hypoperfusion, care must be taken in administering ketorolac. Close attention to urine output and parameters of renal function must be maintained. Moreover, postoperative ketorolac therapy should be avoided in patients who have conditions that predispose to NSAID nephrotoxicity (as in our Case 1). Likewise, in nonsurgical patients the same degree of caution should be used with ketorolac as with any oral NSAID. Finally, since ketorolac is excreted almost entirely by the kidney, either elderly patients or patients with underlying renal insufficiency must have an adjustment of the dosing interval, or this medication should be avoided in such patients altogether.

Acute Kidney Injury↗
PubMed1993

Posttransplant erythrocytosis: case report and review of newer treatment modalities.

A case of posttransplant erythrocytosis in a 51-year-old diabetic man is described. This problem, which can occur in 5 to 15% of renal transplant patients, can result from a contracted plasma volume (diuretics, pressure natriuresis, or glycosuria) or from a true elevation in red blood cell mass. Once the diagnosis of true erythrocytosis is made by a radiolabeled red blood cell mass study, secondary causes such as hypoxia, liver disease, polycythemia rubra vera, renal artery stenosis, and cystic kidney disease should be excluded. Posttransplant erythrocytosis has only been observed in renal transplant recipients and appears to be more frequent with cyclosporine compared with azathioprine therapy. An inappropriately high level of erythropoietin has been described in some, but not all patients, suggesting stimulation of erythropoietin production as the mechanism. Posttransplant erythrocytosis can be associated with an increased incidence of thrombotic events. The presence of this potential complication has prompted intervention to maintain the hematocrit below 50 to 55%. Measures such as discontinuation of diuretics as well as better control of blood pressure and plasma glucose should be used to facilitate the correction of extracellular volume contraction. Phlebotomy has been the most accepted intervention to intermittently lower the hematocrit when needed, but this can lead to iron deficiency. Newer therapeutic modalities are now being used to treat the problem medically. Theophylline, which reduces adenosine-mediated erythropoietin synthesis, is effective but may be associated with side effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Volume↗
PubMed1991

Can ibuprofen cause acute renal failure in a normal individual? A case of acute overdose.

The nonsteroidal antiinflammatory drug (NSAID), ibuprofen, is associated with several renal syndromes, including acute renal failure. NSAID-induced acute renal insufficiency is thought to occur almost exclusively in clinical situations where maintenance of renal blood flow (RBF) is prostaglandin-dependent. However, we present a case of acute renal failure with tubular necrosis occurring as the apparent result of ibuprofen overdose in a patient with no predisposition to NSAID-induced renal failure.

Drug Overdose↗
PubMedDate not supplied

Trimethoprim is a potassium-sparing diuretic like amiloride and causes hyperkalemia in high-risk patients.

Trimethoprim-sulfamethoxazole is a commonly prescribed antimicrobial agent. Twenty-five years after its introduction into clinical practice, an unrecognized and potentially lethal adverse reaction associated with trimethoprim-sulfamethoxazole therapy, hyperkalemia, was described. Both "high-dose" and "standard-dose" trimethoprim-sulfamethoxazole have been associated with this electrolyte disorder. Recognition of this potassium disturbance led to the subsequent description of the mechanism by which trimethoprim-sulfamethoxazole induced hyperkalemia. Trimethoprim was found to act like the potassium-sparing diuretic amiloride and reduce renal potassium excretion. Hence, trimethoprim is in fact a potassium-sparing diuretic like amiloride and causes hyperkalemia in high-risk patients.

Anti-Infective Agents↗
PubMedDate not supplied

Acute renal failure after cardiac transplantation: a case report and review of the literature.

Acute renal failure (ARF) is a relatively frequent complication associated with heart transplantation. It develops in the first few days postoperatively and is characterized by oliguria with laboratory and urinary indices typical of pre-renal azotemia. Cyclosporine, especially with higher doses, is one of the many factors which play an integral part in the nephrotoxicity following cardiac transplant. Poor preoperative renal function and perioperative hemodynamic compromise may also contribute to ARF. The actual incidence of ARF now encountered by transplant centers may be lower than previously reported, the result of lower cyclosporine doses. Currently, management is entirely supportive, but novel therapeutic approaches with atrial natriuretic peptide-like substances are being explored. A case illustrating the typical clinical presentation of ARF after heart transplant will be presented and the clinical features will be reviewed.

Acute Kidney Injury↗