Donald A. Feinfeld

Hypertensive encephalopathy and the neurologic manifestations of malignant hypertension

In a prospective study, 34 patients with 41 admissions for malignant hypertension were examined by a neurologist before and after antihypertensive treatment. Neurologic examination was normal in 17 cases, and neurologic diagnoses in 19 others included acute cerebral infarction (10), uremic encephalopathy (4), dementia of uncertain etiology (3), multiple infarct dementia (1), and chronic paranoid schizophrenia (1). Five patients had a generalized neurologic syndrome consistent with hypertensive encephalopathy, characterized by altered mental function with or without generalized convulsions. In these patients, neurologic examination was normal 1 to 7 days after lowering of blood pressure, while renal function remained unchanged. Neurologic disease is therefore common in malignant hypertension, and hypertensive encephalopathy may be more frequent than previously described.

Acute Renal Dysfunction in Acetaminophen Poisoning

Although acetaminophen (APAP)-associated liver injury is well recognized, there are few reports describing APAP nephrotoxicity, and most of them are single cases. It has also been suggested that N-acetylcysteine (NAC), used to treat the hepatotoxicity, may be harmful to the kidneys. To examine this contention and to determine whether renal involvement in APAP poisoning is at all common, we analyzed the incidence and outcome of acute renal dysfunction in patients hospitalized for APAP overdose reported to our regional poison center over a year. Eleven APAP-poisoned patients had elevated liver function tests; nine of them had azotemia. Those with higher AST levels tended to be younger and to have lower APAP levels on admission. Two patients with acute renal injury died after admission. The other seven patients with renal dysfunction recovered in 2 to 7 days. Six of these received NAC; their mean serum creatinine fell from 3.2 ± 2.0 versus 1.7 ± 0.9 mg/dL (p < 0.05). We conclude that acute renal failure is not uncommon in APAP poisoning and appears to be unrelated to the degree of liver injury. NAC therapy did not seem to worsen nephrotoxicity.

Nephrotic Syndrome Associated with Use of the Nonsteroidal Anti-Inflammatory Drugs

Although acute interstitial nephritis associated with the use of nonsteroidal anti-inflammatory drugs has long been recognized, only recently has its association with ‘minimal change’ nephrotic syndro

Nephrotic-range proteinuria in patients with renovascular disease

Abstract PURPOSE: Proteinuria is usually considered a manifestation of glomerular disease. We sought to describe the characteristics of patients with nephrotic-range proteinuria resulting from renovascular disease and to compare them with those of patients who had glomerulonephritis. SUBJECTS AND METHODS: We identified 14 patients with nephrotic-range proteinuria and renovascular disease and compared them with 14 patients who had nephrotic-range proteinuria and biopsy-proven glomerulonephritis, matched for sex, age, and glomerular filtration rate. RESULTS: Patients with renovascular disease were more likely to have known atherosclerotic vascular disease [13 of 14 (93%) vs 3 of 14 (21%), P P P P P = 0.005), and plasma aldosterone concentration (40 ± 23 vs 11 ± 10 ng/dL, P = 0.0001); and lower serum potassium levels (3.3 ± 0.5 vs 3.8 ± 0.5, P 3 ) and filtration fraction was markedly greater (0.28 ± 0.04 vs 0.15 ± 0.07, P = 0.0001) in the patients with renovascular disease. After the oral administration of captopril, blood pressure, effective renal plasma flow, and glomerular filtration rate decreased only among patients with renovascular disease. Of the 14 patients with renovascular disease, 13 had evidence of renal artery thrombosis seen at angiography; 2 patients required dialysis, and 3 others died during follow-up. CONCLUSION: Our findings suggest that the patients with nephrotic-range proteinuria resulting from renovascular disease have distinct characteristics and a poor prognosis.

Prediction of acute renal failure by bedside formula in medical and surgical intensive care patients

Background: Prediction of which intensive care unit (ICU) patients are likely to develop acute renal failure (ARF) would be useful. However, scoring systems such as APACHE have been disappointing in this regard. We previously developed a bedside formula to predict ARF using only 3 parameters: serum albumin, urine osmolality, and presence of sepsis. Methods: We prospectively evaluated 115 consecutive medical ICU (MICU) patients, comparing the bedside formula to APACHE II AND APACHE III as predictors of ARF or death and looking at nutritional parameters such as iron binding capacity, triceps skin fold, mid-arm circumference, and total lymphocyte count. We then evaluated 123 additional consecutive MICU and 98 consecutive surgical ICU (SICU) patients, comparing the bedside formula to APACHE II. Results: The bedside formula was consistently more accurate than APACHE II in predicting ARF or in-hospital death in MICU patients. However, in SICU neither formula predicted ARF, and APACHE II predicted in-hospital death slightly better. No nutritional parameter other than albumin correlated with ARF. Conclusion: The bedside formula appears superior to APACHE II in predicting ARF or death in MICU but not SICU. This suggests that these two ICU populations are different.

Use of ‘Locked-In’ Antibiotic to Treat an Unusual Gram-Negative Hemodialysis Catheter Infection

A 37-year-old woman on maintenance hemodialysis for 3 years had multiple vascular access failures due to antiphospholipid syndrome. She was dialyzed via a tunneled left subclavian catheter, but after 1 year developed chills and fever during each dialysis session. Blood cultures grew out Xanthomonas maltophilia sensitive to ceftazidime and ciprofloxacin. Intravenous administration of both antibiotics failed to eradicate infection. We added ‘locked-in’ ceftazidime, instilling it daily into the catheter along with heparinized saline for 3 weeks. Within 24 h the patient was dialyzed uneventfully, and all subsequent blood cultures have been negative. This case shows the successful use of a ‘locked-in’ antibiotic to treat an unusual gram-negative catheter infection. Two prior series have reported similar good results in infections with more common organisms. Such treatment may permit continued use of tunneled hemodialysis catheters for longer periods.

Tubulointerstitial nephritis associated with minimal self reexposure to rifampin

We report the case of a 27-year-old Asian man who self-medicated with two capsules of rifampin 1 year after completing a continuous course of chemotherapy for tuberculosis that included that drug. He developed flank pain and edema and presented with uremia requiring dialysis; despite this, he had a serum potassium of only 3.5 mEq/L. Renal biopsy showed interstitial infiltrate with inflammation of the tubules. Renal function began to improve after a 3-week course of prednisone. This case is remarkable for the severity of the renal failure despite such a minimal self-exposure.

A Prospective Study of Urinary Ligandin in Patients at Risk of Renal Tubular Injury

The urinary excretion of ligandin, a proximal tubular enzyme and binding protein, was measured by radioimmunoassay in eight normals, six patients receiving radiocontrast media, and six patients in a critical care unit who were considered at high risk for acute renal failure. Ligandinuria was found to occur normally at rates under 5 micrograms/hr. In the patients receiving radiocontrast media, abnormal rates of ligandinuria were found in four patients. In 102 ligandin measurements in the critically ill patients, rates of ligandinuria exceeded normal only once (after contrast media exposure) despite 13 identifiable episodes of potentially nephrotoxic circumstances and two episodes of acute renal failure. Ligandinuria appears more sensitive as a marker for tubular injury from contrast media than from other renal insults.

Myoglobinuria in Chronic Renal Failure

Serum and urine myoglobin levels were determined on 14 patients with stable chronic renal failure. Serum myoglobin ranged from 38 to 350 ng/mL. Eleven patients had myoglobinuria between 15 and 250 ng/mL; none developed myoglobinuric renal failure. Fractional excretion of myoglobin in the myoglobinuric patients increased as creatinine clearance decreased, although there was no correlation between filtered load and excretion rate of myoglobin. This confirms that renal failure leads to hypermyoglobinemia and usually to myoglobinuria. Surviving nephrons tend to reabsorb less of the filtered load of myoglobin as renal function diminishes.

Erythrocyte Sodium and Potassium in Patients on Peritoneal Dialysis

Intracellular sodium and potassium concentrations were determined on erythrocytes obtained, before and after treatment, from patients with end-stage renal disease undergoing 48-hour intermittent peritoneal dialysis. Erythrocyte sodium increased from 7.5 +/- 0.3 to 8.6 +/- 0.4 mmol/L cells with a mean of 1.1 +/- 0.1 mmol/L cells (P less than .001), but erythrocyte potassium and cellular water content were virtually unchanged. Plasma potassium decreased during dialysis from 4.2 +/- 0.2 to 3.3 +/- 0.1 mEq/L (P less than .001). The increase in red-cell sodium correlated with this decrease in plasma potassium (r = .51, P less than .01). In contrast, erythrocyte sodium and potassium in undialyzed control patients with chronic renal failure did not change over a similar period, and plasma potassium was unchanged (4.3 +/- 0.1 mEq/L before and 4.3 +/- 0.2 mEq/L after 48 hours). Incubation of postdialysis erythrocytes from the dialysis patients in their own plasma at varying potassium concentrations showed that the rise in cell sodium was blunted as the plasma potassium was increased from 3.2 +/- 0.1 to 4.5 +/- 0.2 mEq/L. These results suggest that unlike hemodialysis, which is not associated with short-term changes in red-cell electrolytes, intermittent peritoneal dialysis results in a reversible increase in erythrocyte sodium. This change appears to be causally related to the decrease in extracellular potassium concentration.