Renal complications after heart transplantation.
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Cyclosporine↗
Biomedical subjects
W M Bennett
Publications and source records attributed to W M Bennett.
Pericardial effusions associated with minoxidil.
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Adolescent↗
An animal model of chronic cyclosporine nephrotoxicity.
The development of a reproducible animal model that mimics CSA nephropathy in man has allowed the examination of the several proposed mechanisms of toxicity. While the precise mechanism remains to be defined, important clues have been provided and creative techniques for minimizing the adverse effects of this very valuable adjunct to transplant success have been identified.
Animals↗
Long-term minoxidil therapy in patients with refractory hypertension and renal disease.
Minoxidil, an orally effective vasodilator, was successful in lowering blood pressure in 22 patients, followed up for up to 3 yrs, with hypertension refractory to medical management, including both antihypertensive drug combinations and ultrafiltration. In nondialysis patients renal function was preserved and in dialysis patients bilateral nephrectomy was avoided. Although sodium retention and reflex tachycardia were common, they were managed by beta-adrenergic blockade with propranolol and diuresis with furosemide.
Adolescent↗
Fatal pulmonary bleomycin toxicity in cisplatin-induced acute renal failure.
A 53-year-old male being treated for a metastatic squamous cell carcinoma had fatal pulmonary toxicity as a result of bleomycin therapy. The toxic reaction was observed when the conventional dose regimen of bleomycin was given to the patient who had unrecognized cisplatin-induced acute renal failure. Bleomycin dosage should be reduced in patients with established acute renal failure and the combination of cisplatin and bleomycin should be carefully followed.
Acute Kidney Injury↗
Acute renal failure in toxic shock syndrome owing to rhabdomyolysis.
Toxic shock syndrome is frequently complicated by renal dysfunction. The mechanism of this functional disturbance is unclear. The present report concerns a 33-year-old woman with reversible renal failure in the course of toxic shock syndrome owing to rhabdomyolysis. It is suspected that the renal consequences of muscle injury play a pathophysiological role in the acute renal failure of toxic shock syndrome.
Acute Kidney Injury↗
Prednisone alters the histopathology of chronic cyclosporine nephropathy.
The effects of prednisone (Pred) and azathioprine (Aza) on a rat model of chronic cyclosporine (CsA) nephropathy were studied. Twenty-four salt-depleted Sprague-Dawley rats were randomized to four groups: (1) control; (2) CsA 15 mg/kg; (3) CsA/Aza 5 mg/kg, and (4) CsA/Pred 1 mg/kg. After 4 weeks, functional measurements, including urinary N-acetyl-beta-D-glucosaminidase (NAG) levels, were determined. Semiquantitative grading of cortical and medullary damage was done. Cross-sectional areas of medullary thick ascending limbs (mTAL) and collecting ducts (CD) were determined. Tubulointerstitial injury was equivalent in all CsA groups, but tended to be lowest in the CsA/Pred group. Mean mTAL size in the CsA/Pred group was significantly greater than controls (p = 0.035). In contrast, mean CD size was not different among all groups. All CsA-treated animals had significantly larger hypertrophic mTAL than controls. The degree of hypertrophy was even greater in the CsA/Pred group (p = 0.006 vs. the other CsA-treated groups). Mean mTAL size was found to correlate with creatinine clearance, free water reabsorption, and urinary NAG. The percent of hypertrophic mTAL was found to correlate with creatinine clearance, free water reabsorption, and urinary NAG. This report shows that Pred alters the nephrotoxic effect of CsA, permitting a predominantly hypertrophic, rather than atrophic, medullary response. The extent of hypertrophy, in all CsA-treated groups, correlated with improved functional parameters, suggesting that at least in one phase of CsA nephropathy compensatory responses preserve renal function.
Animals↗
Interaction between cyclosporine and grapefruit juice requires long-term ingestion in stable renal transplant recipients.
STUDY OBJECTIVE: To examine the effect of the concurrent administration of increasing amounts of grapefruit juice, an inhibitor of drug metabolism, on the steady-state pharmacokinetics of cyclosporine. DESIGN: Open-label, three-period crossover, food-drug interaction study in stable renal transplant patients. SETTING: A university-affiliated clinical research center. PATIENTS: Sixteen stable renal transplant recipients. INTERVENTION: Cyclosporine was administered with 240 ml of water, 240 ml of grapefruit juice, or several 240-ml glasses of grapefruit juice, and serial blood samples were taken to estimate the effect of grapefruit juice on cyclosporine pharmacokinetics. MEASUREMENTS AND MAIN RESULTS: Grapefruit juice caused a significant increase in cyclosporine area under the curve, however, no significant effect was seen in other pharmacokinetic parameters. Grapefruit juice caused an increase in the 24-hour trough cyclosporine concentration, which may be of clinical significance if long-term ingestion of grapefruit juice is recommended. CONCLUSION: A drug interaction exists between cyclosporine and grapefruit juice, and it is likely at the level of intestinal drug absorption.
Adult↗
Analgesic nephropathy and the use of nonsteroidal anti-inflammatory drugs in renal patients: new insight.
Analgesic-associated nephropathy due to analgesic mixtures and possibly due to nonsteroidal anti-inflammatory drugs taken over long periods of time represent a preventable cause of chronic renal failure. The exact prevalence of this condition in various countries around the world is still unclear almost 30 years after the original description of this entity. With the advent of specific diagnostic criteria, the prevalence should become much more clear by studying dialysis populations and other patients with chronic renal disease prior to end stage. The effect of analgesics and nonsteroidal drugs on renal disease of other established etiologies is not well-characterized either. Just as blood pressure control is essential in prolonging the course of chronic renal failure, the use of these NSAIDs may be a risk factor for accelerating such clinical courses. It is of interest that recent preliminary epidemiologic data suggest that prolonged and heavy use of illicit drugs can also be a risk factor for chronic renal disease (personal communication). Such risk factors are compatible with a public health approach towards prevention of a disease state in which expensive resources are necessary and for which the affected population is growing at alarming rates worldwide. Pharmaceutical manufacturers should be required to conduct properly controlled safety studies for long-term effects of compounds, particularly when they are to be released for over-the-counter consumption and are to be heavily marketed.
Anti-Inflammatory Agents, Non-Steroidal↗
Interaction between tacrolimus and nefazodone in a stable renal transplant recipient.
Tacrolimus (FK-506) is an important immunosuppressive agent most often given for maintenance immunosuppression to prevent acute cellular organ rejection. A 57-year-old woman with end-stage renal disease presumed secondary to chronic glomerulonephritis underwent a living related renal allograft transplantation. She tolerated the surgery well and was discharged on postoperative day 5. She was stabilized with prednisone, azathioprine, and tacrolimus. Two years after transplantation, nefazodone 50 mg twice/day orally was prescribed due to depression. After 1 week of nefazodone therapy the patient experienced headache, confusion, and "gray areas" in her vision, without abnormal ophthalmologic findings. Her serum creatinine was elevated to 2.2 mg/dl (baseline 1.5 mg/dl), and trough tacrolimus level was markedly elevated (> 30 ng/ml). Both tacrolimus and nefazodone are metabolized by the cytochrome P450 (CYP) 3A4 system. We suspect that nefazodone inhibits metabolism of tacrolimus. Coadministration of antidepressant agents such as nefazodone, or any other drug that inhibits the CYP3A4 isoenzyme subfamily, should be anticipated to interfere with tacrolimus metabolism. Monitoring blood concentrations of tacrolimus is vital, and appropriate dosage adjustments are required when the two drugs are administered concurrently to avoid serious interactions such as nephrotoxicity and neurotoxicity.
Antidepressive Agents, Second-Generation↗