American journal of kidney diseases : the official journal of the National Kidney Foundation
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To test the hypothesis that race is a predictor of hypertensive renal disease, we examined a general medicine clinic population of 6,880 hypertensive patients who were treated for at least 1 year (mean, 5.2 years). Their mean age was 55.8 years; 70% were women, 72% were black, and 41% were diabetic (95% type II). Many were already under treatment at the time of enrollment. ⋯ The data draw attention to and elucidate the exceptionally high incidence of renal dysfunction in blacks with or without diabetes. Further, they may explain the inordinate numbers of blacks with hypertension requiring dialysis. Finally, these retrospective data suggest that prospective trials to test the effect of blood pressure and glucose control on the course of renal disease in hypertensive and/or type II diabetic patients are warranted.
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The association of interstitial nephritis, the most common renal lesion in Sjogren's syndrome, to the other manifestations of the disease is unclear. To begin to address this issue, the infiltrating cells in frozen kidney tissues from two patients with interstitial nephritis secondary to Sjogren's syndrome were characterized by indirect immunofluorescence. ⋯ Both kidneys contained nodules of B cells. The increased proportion of OKT4+ T cells in salivary gland and in interstitial renal lesions of Sjogren's syndrome contrasts with some other forms of interstitial renal disease and suggests that the renal and salivary gland lesions have a similar pathogenesis.
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Case Reports
Transient paralysis of upper extremity after percutaneous cannulation of the subclavian vein for hemodialysis.
Two cases of transient paralysis of upper extremity after percutaneous cannulation of the subclavian vein for hemodialysis are presented for the first time. Large amounts of lidocaine used, together with its deep and too lateral administration are responsible for development of this transient complication.
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Case Reports
The urine pH: a potentially misleading diagnostic test in patients with hyperchloremic metabolic acidosis.
The purpose of this case report is to illustrate that the urine pH may be a misleading index in the assessment of the normal renal response to metabolic acidosis. On presentation, the patient had a normal anion-gap type of metabolic acidosis; the cause of the acidosis was gastrointestinal bicarbonate loss. ⋯ However, since the kidneys generated more than 190 mmol of bicarbonate per day (urine ammonium was 190 mmol/d), reduced renal acid excretion was not the cause of the acidosis. Therefore, the urine pH of 6.0 provided a false clue with respect to a renal cause for the acidosis in this setting; in contrast, the urine anion gap provides more reliable information concerning bicarbonate generation by the kidney.
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Patient characteristics, clinical outcomes, and proposed pathophysiologic mechanisms are reviewed in 138 patients reported in the literature to have had ascites associated with end-stage renal disease. Contributing mechanisms may include fluid overload, peritoneal membrane changes (not necessarily related to peritoneal dialysis), hypoproteinemia, and lymphatic drainage disturbances. In 15% of cases, extensive evaluations may reveal an underlying disease. The most effective therapy may be kidney transplantation.