Racial analysis of the volume-renin relationship in human hypertension.

We studied 29 normotensive men (14 black, 15 white) and 36 hypertensive men (27 white, nine black) to examine the association of race with blood pressure, blood volume, and peripheral renin activity (pra). Blood volume was lower in white hypertensive men than in white normotensive men, but was similar in all blacks. When subjects were tested in the supine position, PRA was lower in black normotensive subjects than white normotensive subjects. The PRA did not differ among groups tested in an upright posture, while furosemide-stimulated PRA was lower in hypertensive than normotensive subjects of both races despite lower blood volumes in white hypertensive subjects. Differences of volume and renin measurements appear to reflect basic differences between whites and blacks with essential hypertension. We emphasize the need to consider race in the investigation of human hypertension.

Recovery from rapidly progressive glomerulonephritis. Improvement after plasmapheresis and immunosuppression.

Two patients with rapidly advancing renal insufficiency underwent biopsy and were found to have crescentic glomerulonephritis. Patient 1 demonstrated findings compatible with Goodpasture's syndrome. Crescents were present in 100% of his glomeruli. Patient 2 had findings of immune complex-mediated glomerulonephritis and crescents in greater than 90% of his glomeruli. Both patients were treated with high-dose prednisone, cyclophosphamide, and plasmapheresis. Patient 2 additionally required hemodialysis for a brief period. Renal function improved in both patients and has not deteriorated after follow-up of 14 and 18 months, respectively. Repeated renal biopsies were performed in each patient. Our findings suggest that clinical improvement and histologic healing are possible in rapidly progressive glomerulonephritis despite the initial presence of crescents in every glomerulus.

Urinary kallikrein activity and renal vascular resistance in the antihypertensive response to thiazide diuretics.

To evaluate the mechanism of chronic thiazide diuretic action in hypertension, we treated 19 essential hypertensive white men for 1-month periods on placebo alone and hydrochlorothiazide alone. During therapy, mean arterial pressure (MAP) fell, but radioisotopically determined intravascular volume remained unchanged, suggesting other mechanisms of thiazide action upon blood pressure. In the renal circulation, thiazides did not change renal plasma flow or glomerular filtration rate, but renovascular resistance was diminished, probably at the afferent arteriole. Concomitant with the decline in blood pressure and renovascular resistance, urinary kallikrein excretion increased, from subnormal (hypertensive) levels back into the normal range. The kallikrein increase did not correlate with changes in plasma aldosterone. In addition, patients with blood pressure responses (reduction greater than or equal to 10%) to thiazides (n = 12) had greater increases in kallikrein excretion than those without such a blood pressure decrement (n = 7), suggesting a role for renal kallikrein in the hypotensive response to thiazide diuretics.

Renal hemodynamic changes during long-term antihypertensive therapy.

Studies of renal hemodynamics were carried out in 84 patients with essential hypertension during long-term antihypertensive therapy with a number of drugs. Renal perfusion was maintained or enhanced despite a fall in mean arterial pressure during therapy with hydrochlorothiazide, furosemide, clonidine, prazosin, and the combination of guanabenz and hydrochlorothiazide. Renal perfusion deteriorated during long-term treatment with propranolol. Renal hemodynamics may be enhanced, maintained, or adversely influenced depending on the choice of antihypertensive agent.

Exogenous protein as the cause of nephrotic-range proteinuria.

Hematuria and proteinuria developed in a young woman with waxing and waning symptoms suggestive of systemic lupus erythematosus. Quantitatively, the proteinuria was in the nephrotic range, but other manifestations of the nephrotic syndrome were absent. Serologic evaluation demonstrated normal results. The hematuria was subsequently found to be self-induced and related to foreign objects in the bladder. Urine protein electrophoresis confirmed severe proteinuria with a spike in the gamma region. Immunoelectrophoresis demonstrated that the proteinuria was not of human origin. Subsequent urinary protein values were normal. This case exhibits features compatible with Münchausen's syndrome and shows that severe proteinuria may be factitious.

Baroreflex dysfunction in patients with adult-onset diabetes and hypertension.

Ten patients with adult-onset diabetes in whom diabetes antedated the appearance of hypertension were evaluated. These patients had evidence of diabetic autonomic neuropathy, including significant orthostatic hypotension (four patients), impotence (three patients), and evidence of diabetic peripheral sensorimotor neuropathy (nine patients) in clinical testing and nerve conduction study results. Baroreflex function was evaluated by multiple hemodynamic tests, including inhalation of amyl nitrite and intravenous administration of phenylephrine, before and after parasympathetic blockade with atropine, and the cold pressor test; results were compared with results in normal control subjects, patients with essential hypertension, and two subgroups of uremic patients undergoing maintenance hemodialysis. Baroreflex function was significantly abnormal in the diabetic patients and was consistent with combined parasympathetic and sympathetic motor nerve (efferent) dysfunction in the baroreflex arc. There was a significant inverse correlation between the degree of orthostatic hypotension in the diabetic patients and their baroreflex response to phenylephrine (r = -0.680, p less than 0.05). There was no significant correlation between supine hypertension in the patients with diabetes and any of the hemodynamic or biochemical parameters examined. The results suggest that orthostatic hypotension in these patients is related to baroreflex dysfunction. However, baroreflex dysfunction does not appear to be a factor in the development of hypertension in these patients, although more studies with normotensive diabetic patients are needed to confirm this point.

Ureteral involvement complicating eosinophilic cystitis.

A thirty-three-year-old woman was evaluated for eosinophilia, irritative bladder symptoms, and renal insufficiency. Eosinophilic cystitis was documented by bladder biopsy and glomerulonephritis by renal biopsy. As the glomerulonephritis and other symptoms resolved, unilateral ureteral obstruction developed with irreversible loss of right renal function. The distal ureter was found to have eosinophilic infiltration. This entity should be considered in the differential diagnosis of unilateral ureteral obstruction associated with cystitis.

Renal papillary necrosis in thyroid carcinoma.

A thirty-four-year-old man with progressive visual impairment was found to have thyromegaly and renal insufficiency at the time of admission. Subsequent evaluation demonstrated bilateral optic neuritis and a thyroid nodule which proved to be a follicular carcinoma. Nephrologic studies revealed bilateral papillary necrosis and chronic interstitial nephritis on biopsy. The patient's renal function stabilized and twenty-four-hour protein excretion diminished after hemithyroidectomy. Carcinoma-related protein production may have played a role in the development of the observed renal lesions. Carcinoma should be a consideration in patients with unexplained papillary necrosis.

Nephrotic syndrome. Pathogenesis, clinical and therapeutic considerations.

The nephrotic syndrome is the result of a variety of immunologic mechanisms which damage the glomerular capillary wall and cause excessive protein loss. The great number of potential predisposing factors and clinical settings necessitates a thorough history and a careful examination that includes well-defined laboratory studies. Appropriate therapy covers a broad range, from doing nothing more than reducing additional insults, to the aggressive use of combined modalities, depending on the factors involved in the individual case.

Hypertension in renal insufficiency: a major therapeutic problem.

Hypertension and a high incidence of cardiovascular morbidity and mortality often accompany end-stage renal disease. Causes of the hypertension include abnormalities of extracellular fluid volume, increased activity of the renin-angiotensin system, dysfunction of the autonomic nervous system, and deficiency of vasodilator substances. Treatment is not detrimental to residual renal function and may enhance the quality of survival. Several types of therapy are available that may be used sequentially or in combination. New antihypertensive drugs and improved blood-cleansing devices allow a more optimistic outlook on long-term survival in end-stage renal disease.

Torulopsis glabrata fungemia in a diabetic patient.

We have presented a case of a stable diabetic outpatient who had an acute illness that proved to be Torulopsis glabrata fungemia responsive to amphotericin B therapy. Her only apparent additional predisposition was a nonobstructing renal calculus. Fungemia with this organism in an outpatient is most unusual. T glabrata should be an additional consideration in outpatient as well as inpatient illnesses, especially in diabetic women.

Diabetic neuropathic pain: control by amitriptyline and fluphenazine in renal insufficiency.

Seven patients with diabetes of ten to 24 years' duration and renal insufficiency were treated with fluphenazine and amitriptyline in an attempt to control severe pain in the extremities. Six patients had relief of pain within five days of initiation of therapy. One patient had no pain relief despite mood alteration. The relief of pain persisted whether renal function was stable or declining. This form of therapy is safe and as effective in patients with neuropathic pain and mild to moderate renal insufficiency as in patients with normal renal function.

Hypernatremia in hepatic failure.

The presence of hypernatremia in patients with hepatic failure has not received major attention. We examined the records of 25 patients admitted to the hospital with decompensated liver disease (usually Laënnec's cirrhosis) and found hypernatremia in 15. Probable causes include increased insensible water losses, impairment of water intake due to encephalopathy, and the use of osmotic cathartics with hypotonic enteric losses. Patients in this series showing hypernatremia had a mortality of 87%. Mortality in those without hypernatremia was 60%. The presence of increased serum sodium concentrations in patients with decompensated liver disease is an ominous but correctable abnormality reflecting a disturbance in water balance.

An evaluation of iridology.

Iridology is an analysis of health based on examination of the iris of the eye. One hundred forty-three patients had photographs taken of both eyes. Nine-five patients were free of kidney disease, defined as a creatinine level of less than 1.2 mg/dL (mean, 0.8 mg/dL), and 48 had kidney disease severe enough to raise the plasma creatinine level to 1.5 mg/dL or greater (mean, 6.5 mg/dL). Three ophthalmologists and three iridologists viewed the slides in a randomized sequence without knowledge of the number of patients in the two categories or any information about patient history. Iridology had no clinical or statistically significant ability to detect the presence of kidney disease. Iridology was neither selective nor specific, and the likelihood of correct detection was statistically no better than chance.

Remission and exacerbation of tumor-related nephrotic syndrome with treatment of the neoplasm.

A 61-year-old man presented with nephrotic syndrome in March 1978. Renal biopsy revealed mesangial and endocapillary proliferation with no underlying cause found. One year later, evaluation of back pain resulted in the finding of undifferentiated adenocarcinoma with compression fracture of the T-11 vertebra. Local irradiation relieved the pain and ameliorated the nephrotic syndrome. In 1981 the nephrotic syndrome recurred. Evaluation revealed metastases to the right pelvis and to the brain without an identifiable primary lesion. Irradiation of these lesions reduced protein excretion to 50 to 150 mg/day. A gastric carcinoma was later found. Exacerbation of nephrotic syndrome may herald exacerbation of tumor activity as occurs in Hodgkin's disease. Survival with tumor-related nephrotic syndrome is not invariably poor, and treatment of metastases may be worthwhile in similar patients in whom only partial tumor reduction is possible.

Rhabdomyolysis, acute renal failure, and disseminated intravascular coagulation in a man with sickle cell trait.

We have described a patient with sickle cell trait who, after severe exertion, had rhabdomyolysis, acute renal failure, and disseminated intravascular coagulation secondary to sickling. Autopsy showed the characteristic histopathology of sickle cell crisis and not terminal sicklemia.

Urinary kallikrein activity in the hypertension of renal parenchymal disease.

To learn more about the regulation of blood pressure in renal parenchymal disease, 57 subjects (18 normal controls, 25 patients with essential hypertension and 14 with renal parenchymal disease and hypertension) were evaluated for peripheral renin activity, 24-hour urinary kallikrein activity and whole-blood volume. Blood volumes were significantly lower in patients with essential hypertension (P less than 0.001) and those with renal disease and hypertension (P less than 0.001) than in normotensive subjects. Renin activities (measured after the subjects were standing) were also lower in patients with essential hypertension and hypertension due to renal disease (P less than 0.01 and P less than 0.02, respectively). Kallikrein activity was similar in subjects with renal disease and those with hypertension (P less than 0.05) but markedly diminished in both groups as compared with normotensive subjects (P less than 0.001 and P less than 0.01, respectively) when glomerular filtration rates were taken into account. The kallikrein-kinin system may be involved in the hypertension associated with renal parenchymal disease.

Hepatic coma after open heart surgery.

Fulminant hepatic failure has been reported in patients with chronic congestive heart failure. Two patients in whom jaundice and coma followed cardiac surgery were studied to find the possible etiology. Clinical, biochemical, and histologic evaluations revealed low cardiac output; elevated levels of bilirubin, lactic dehydrogenase, serum glutamic oxaloacetic transaminase, and alkaline phosphatase; prolonged prothrombin time; and centrizonal necrosis of hepatocytes with sinusoidal dilatation. No other possible causes of hapatic dysfunction and coma were identified. We conclude that acute postoperative congestive heart failure may cause fulminant hepatic failure and metabolic encephalopathy.