Sudhir K. Anand

Hypertension secondary to a renin-producing juxtaglomerular cell tumor

1. Strauss HW, Harrison K, Langan JK, Lebowitz E, and Pitt B: Thallium-201 for myocardial imaging: relation of thallium-201 to regional myocardial perfusion, Circulation 51:641, 1975. 2. Hamilton GW, Trobaugh GB, Ritchie JL, Williams DL, Weaver WD, and Gould KL: Myocardial imaging with intravenously injected Thallium-201 in patients with suspected coronary artery disease. Analysis of technique and correlation with electrocardiographic coronary anatomic and ventriculographic findings, Am J Cardiol 39:347, 1977. 3. Weich HF, Strauss HW, and Pitt B: The extraction of thallium-201 by the myocardium, Circulation 56:188, 1977. 4. Ferrer PL, Gottlieb S, Garcia OL, and Miale A: Noninvasive diagnosis of anomalous left coronary artery in the young with thallium-201 myocardial imaging, Pediatr Res 11:389, 1977 (abstr). 5. Wesselhoeft H, Fawcett JS, and Johnson AL: Anomalous origin of the left coronary artery from the pulmonary trunk. Its clinical spectrum, pathology and pathophysiology based on a review of 140 cases with seven further cases, Circulation 38:403, 1968. 6. Venugopal P, and Subramanian S: Anomalous origin of the left coronary artery from the pulmonary artery. Definitive surgical treatment by saphenous vein interposition in a 17 month old child, Ann Thorac Surg 19:451, 1975. 7. Neches WH, Mathews RA, Park SG, Lenox CG, Zuberbuhler JR, Siewers RD, and Bahnson HT: Anomalous origin of the left coronary artery from the pulmonary artery. A new method of surgical repair, Circulation 50:582, 1974. 8. El-Said GM, Ruzyllo W, Williams RL, Mullins CE, Hallman GL, Cooley DA, and McNamara DG: Early and late results of saphenous vein graft for anomalous origin of left coronary artery from pulmonary artery, Circulation 48:11 l, 1973. 9. Chiariello L, Meyer J, Reul GJ, Hallman GL, and Cooley DA: Surgical treatment for anomalous origin of left coronary artery from pulmonary artery and cardiovascular surgery, Ann Thorac Surg 19:443, 1975. 10. Strauss HW, Pitt B, Rouleau J, Bailey IK, and Wagner HN: Atlas of Cardiovascular nuclear Medicine, St. Louis, 1977, The CV Mosby Company, pp 128-129.

Pseudohypoaldosteronism due to sweat gland dysfunction.

Extract: Pseudohypoaldosteronism is an uncommon disorder characterized by urinary sodium wasting and is attributed to a defect in distal renal tubular sodium handling with failure to respond to endogenous aldosterone. Sweat electrolyte values in other reported patients, when measured, have been normal. A 3.5-year-old girl developed repeated episodes of dehydration, hyponatremia, and hyperkalemia during the first 19 months of life. Serum sodium was as low as 113 mEq/liter and potassium as high as 11.1 mEq/liter. Her plasma and urinary aldosterone levels were persistently elevated (Figs. 1–4). Unlike patients with classic pseudohypoaldosteronism she demonstrated no urinary sodium wasting (Figs. 2 and 3). During episodes of hyponatremia and reduced sodium intake her urinary sodium was less than 5 mEq/liter. In addition, her sweat sodium concentration was consistently above 125 mEq/liter and salivary sodium concentration above 58 mEq/liter. Her chest x-ray, 72-hr fecal fat excretion, serum and urinary pancreatic amylase (amy-2) were normal, providing no evidence for cystic fibrosis. It is proposed that this patient represents a new variant of pseudohypoaldosteronism with excessive loss of sodium from the sweat and salivary glands instead of the kidneys.Spectulation: Aldosterone is known to control sodium and potassium excretion by kidneys, sweat glands, and salivary glands. In patients with classic pseudohypoaldosteronism there is a defect in renal tubular response to aldosterone action. Studies in the present patient suggest that there may be variants of this syndrome in which the end organ defect is in the sweat and salivary glands instead of the renal tubule. In addition, it is possible that new variants will be found in which end organ defect is in still other organs concerned with electrolyte transport.

The Effect of Chronic Furosemide Administration on Urinary Calcium Excretion and Calcium Balance in Growing Rats

Summary: This study was designed to determine the calciuretic effect of furosemide and its impact upon calcium balance during chronic (25 days) furosemide administration to growing rats. Experiments were performed on 18 six-wk-old rats. Nine animals received furosemide, and 9 served as controls. The administration of furosemide in a dose of 40 mg resulted in a significant increase in calcium excretion in the treated group; urinary calcium excretion almost doubled that of the controls during the first 24-hr collection (3.74 ± 0.44 mg in the treated animals compared with 1.90 ± 0.15 mg in the controls; P < 0.05). The average daily urinary calcium excretion during each of four subsequent 6-day periods remained approximately three-fold higher in animals which received furosemide compared with controls (P < 0.001 for each 6-day period). The furosemide-induced increase in urinary calcium excretion did not diminish with time. Sodium excretion did not significantly increase either acutely or chronically in response to furosemide. Daily urinary volume increased approximately 40 to 60% in the furosemide-treated group compared with that of the controls (P < 0.001). The cumulative calcium balance in the control group exceeded by 7% that of the furosemide-treated animals (2696.3 ± 20.8 mg versus 2518.6 ± 20.1 mg (P ±.001).The findings indicate that distal nephron compensatory mechanisms effecting sodium conservation following furosemide do not result in similar conservation of calcium. Calcium balance may be deleteriously affected.Speculation: The long-term effects of furosemide on calcium homeostasis in man are not known. This study in rats suggests that furosemide may have deleterious effects on calcium homeostasis. Similar effects in humans, particularly growing children, may result in decreased calcium balance and bone demineralization.

Persistent hypernatremia due to abnormal thirst mechanism in a 13-year-old child with nephrogenic diabetes insipidus

A 13-year-old mentally retarded boy with the clinical features of Prader-Willi syndrome and Pitressin-resistant polyuria was found to have persistent hypernatremia despite free access to water. His total body water, extracellular fluid, and plasma volume were reduced, and peripheral venous renin activity was increased. He drank 6 to 8 liters of fluid per 24 hours but still had a blunted thirst response as reflected by changes in serum sodium concentration, which varied as much as 12 mEq. per liter from morning to evening. His chronic hypernatremia is regarded as due to deranged thirst regulation and dehydration.

459 INCREASED PLANT INGESTIONS 1963|[ndash]|1977: A PROBLEM OF HOME SAFETY ASSOCIATED WITH THE BACK TO NATURE MOVEMENT

This study examines if the “back to nature” movement which started in the 1960s has resulted in increased buying of plants by the American public and if there has been a concomitant increase in plant ingestions. Sales of retail nursery stores for 1963,67,72, and 77 for the United States (US) recorded by the US Dept of Commerce census of retail trade are: (Amounts in thousands and corrected for inflation to 1967 constant

CHANGES IN GLOMERULAR BASEMENT MEMBRANE(GBM) ANTIGEN(S) WITH AGE AND DISEASE

):For the same years the incidence of plant ingestions (except mushrooms) in children < 5 years old recorded by National Clearing House for Poison Control Centers is:These data indicate that the US public has been buying more plants which has altered the home environment. This fact, very likely has resulted in increased plant ingestions by young children. Improved public education regarding safe and poisonous plants may reduce the incidence of poisonous plant ingestions.

Diagnosis of hereditary nephritis by failure of glomeruli to bind anti-glomerular basement membrane antibodies

GBM of patients with Alport Syndrome(AS) does not bind anti-GBM (McCoy et al, Lab Invest 3:19, 1976). Diagnostic use of staining kidney biopsies of AS suspect children with antiGBM was evaluated. Kidneys of 21 autopsied patients without renal disease (Groups I-III) and 3 patients with AS (with characteristic electron microscopic lesions) were treated with serum of a patient with strong antiGBM, then with fluorochromed anti IgG. Results were as follows:Young infants, like AS patients, appear to lack GBM antigen(s) normally present in older children and adults. Normal GBM increases from 950 Å at birth to 2844 Å by 3 years. Whether adult components are superimposed on fetal GBM or fetal GBM is replaced by adult GBM components is unknown. Failure of GBM to bind antiGBM is not diagnostic of AS in young infants, but is useful in older patients. These data may also partly explain absence of antiGBM nephritis in young children.