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Hypertension leads to renal disease through a series of mechanisms that seem to be exaggerated in African-Americans, who have a higher prevalence of both hypertension and end-stage renal disease than whites. Renal disease itself leads to hypertension, which in turn can contribute to progression of renal disease. Although there are numerous mechanisms involved in the process of renal disease progression, the renin-angiotensin system plays a major role as determined by the beneficial response to angiotensin I-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (AT II blockers) of reduced rate of progression in a variety of clinical and experimental renal diseases. Macromolecular trafficking across the glomerulus leading to proteinuria plays a significant role in progression of chronic renal disease. Reversal of this abnormality and reduced stress on capillary walls may be the major mechanisms of beneficial action of ACEIs and AT II blockers in halting renal disease progression.

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In the past few years, increased knowledge of the nature of transport proteins and their molecular regulation in the translocation of ions across kidney membranes has emerged. We are beginning to better understand the characteristics of the interaction of diuretics with these transport proteins. It is likely that this knowledge will permit further insight into nephron function regulation.

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Necrosis of the outer two-thirds of the cortex (CN) was induced with boiling water in the left kidney of rats. Two days afterward, morphological damage was shown to be limited to the superficial cortex; deep nephron population was well-preserved. Glucose reabsorption under basal and glucose loading conditions, and extraction of p-aminohippurate, used as indices of proximal tubule integrity, were normal in control and experimental kidneys 48 h after cortical necrosis. Basal fractional water and electrolyte excretion did not differ between control and experimental kidneys. Calculated mean single-nephron glomerular filtration rate (GFR) and plasma flow for superficial (SupGFR and SupNPF) and juxtamedullary nephrons (JMGFR and JMPF) were similar to those obtained by micropuncture and Hanssen's technique for SupGFR, and for JMGFR by Hanssen's. Volume expansion led to a 27% increase in calculated SupGFR, but no change in JMGFR. The JMPF increased by 81%, whereas SupNPF increased by only 23%, suggesting that, in this model, GFR of deep nephrons may be independent of plasma flow. The results indicate that deep nephrons retain their functional integrity 48 h after cortical necrosis. After volume expansion fractional excretion of sodium was greater, and fractional water reabsorption less, in CN than in control kidneys. Thus handling of sodium and water by superficial and deep nephrons under basal conditions was similar, but reabsorptive capacity for deep nephrons of CN was lower during volume expansion. The present studies suggest that deep nephrons can maintain relatively normal function in cortical necrosis.

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Various studies have shown that a high protein (HP) diet, compared to a low protein (LP) diet, leads to hypercalciuria and alterations in renal and systemic hemodynamics. The authors compared the effects of HP diet to those of normal protein diet (NP) to determine the possible mechanisms by which changes in systemic hemodynamics and hypercalciuria occurred. The studies were conducted in awake rats; the effects of dietary sodium content on the changes induced by HP also were evaluated. The relationship of prostaglandins (PG), renin (PRA), and aldosterone (PA) to changes in blood pressure (BP) was assessed. Two weeks after HP and normal sodium feeding (40%), glomerular filtration rate (GFR) and urine flow (V) were not different from the same values in a group on an NP diet (23%). When HP was fed with low sodium, there was a rise in V as a consequence of greater fluid intake. Although plasma calcium remained constant, the hypercalciuria correlated with high protein and sodium content. Alterations in 1,25(OH)2 vitamin D3 or PTH (cyclic AMP excretion) function did not explain the hypercalciuria induced by HP. This suggests that HP leads to inhibition of tubular calcium reabsorption by mechanism(s) yet to be elucidated. Although HP did not alter GFR, it led to an increase in BP, a fall in renal vascular resistance, and an increase in RPF, regardless of sodium intake. PRA and urine PGE2 excretion were significantly higher in the rats on HP diet, whereas PA remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

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The relationship between hyperuricemia, gout, and autosomal dominant polycystic kidney disease (ADPKD) is not widely recognized. In an attempt to further clarify this relationship, the authors have studied 17 patients with ADPKD, 9 controls, 9 patients with proven gout and chronic renal failure, 11 patients with gout and normal renal function, and 11 patients with chronic renal failure. The mean serum uric acid concentration was higher in patients with ADPKD as a group than in controls (8.0 +/- 1.7 mg/dl vs. 6.4 +/- 1.6 mg/dl, p less than .02). Clinical gout was identified in 24% of patients with ADPKD; none of the patients with chronic renal failure of other etiologies had gout. Fractional excretion of uric acid and the activity of the enzyme hypoxanthine guanine phosphoribosyl transferase (HGPRT) were not different among the groups studied. From this study the authors conclude that ADPKD should be included among those diseases associated with hyperuricemia and gout. A partial deficiency in HGPRT or abnormal renal handling of uric acid do not appear to be responsible for the increased incidence of gout in patients with ADPKD.

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We have previously reported a high incidence of cataract formation in adult hypertensive salt-sensitive rats, suggesting that hypertension may be an important cataractogenic risk factor. Weanling salt-sensitive rats that eventually developed cataracts showed a marked increase in the pressor response to a high-sodium diet compared to salt-sensitive rats that did not develop cataracts. A lens and aqueous fluid electrolyte imbalance occurred in all adult salt-sensitive rats examined, but was greater in the salt-sensitive rats that developed cataracts, suggesting an alteration in lens and/or ciliary ion transport in cataracts associated with hypertension. In the present study, lens 86Rb uptake was measured in adult hypertensive salt-sensitive rats prior to cataract formation. 'Cataract-prone' salt-sensitive hypertensive rats (increased pressor response to a high sodium diet given at weanling age), salt-sensitive hypertensive rats unlikely to develop cataracts and control salt-resistant rats were studied at the age of 16 weeks. Total and ouabain-insensitive lens 86Rb uptake were measured for the determination of ouabain-sensitive uptake, an index of Na+,K+-ATPase activity. Lens ouabain-sensitive 86Rb uptake was low in adult hypertensive cataract-prone salt-sensitive rats before cataract formation compared with values in control resistant rats. Intermediate values were observed in hypertensive salt-sensitive rats unlikely to develop cataracts. These data suggest that altered ion transport may play a pivotal role in cataractogenesis associated with this model of hypertension. The data are also consistent with the concept of a generalized defect in epithelial ion transport, at least in salt-sensitive hypertension.

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Despite renal involvement in the genesis of hypertension, the precise renal hemodynamic events prior to and during development of hypertension have not been obtainable by direct study in the available rat models of genetic hypertension. We have developed a model of genetic salt-sensitive hypertension in rats with superficial glomeruli, using the protocol described by Dahl to develop the Brookhaven model. Adult Munich Wistar rats were purchased from Charles River and bred in our laboratory. Offspring were allowed to mature without intervention. Systolic blood pressure and body weight were measured weekly to determine the normal longitudinal changes with increasing age for this strain. Balance studies were also carried out longitudinally, and during these studies plasma renin activity (PRA) was determined. When the rats were 16 weeks old, the availability of superficial glomeruli was assessed under microscopic examination and only those rats with numerous superficial glomeruli/field were mated. The offspring of these breeders were used as the zero generation (F0) of salt-sensitive rats, and were treated as described by Dahl. Systolic blood pressure, body weights and balance studies were carried out in this and in all subsequent generations. Sibling breeding was maintained and rats were bred for salt-sensitivity (systolic blood pressure greater than 155 mmHg at the age of 2 months) and availability of superficial glomeruli. Those rats with systolic blood pressure of less than 120 mmHg were bred in an attempt to develop a salt-resistant strain, and untreated Munich Wistar rats were bred to provide another control.(ABSTRACT TRUNCATED AT 250 WORDS)

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In this cross-cultural study of Puerto Rican and Texas physicians, we have tested the hypothesis that physicians' "humanistic attributes" are culturally related. Differences (P = .05 to .01) were found between mean responses of the two groups of residents to seven of the questions on the Totalitarian-Authoritarian-Dogmatism scale. Factor analysis determined that the two principal components of disagreement were medical political and ethical issues (P = .001) but not patients and their problems. Faculty responses provided additional evidence that customs and traditions influence how professional subgroups manifest attitudes: Puerto Rican faculty rated residents highest on "humanistic traits" if they self-reported high ethical scores, and lowest if they self-reported high radical scores; Baylor faculty reflected the "age-drag" on changing values by differing (P = .05 to .001) from both groups of residents on 38% of the questions. The difficulty of rating residents with a universal standard of "humanistic traits" is supported by the culture and age-specific differences reported herein.

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We have studied 83 patients with recurrent calcium stone formation in an attempt to determine an approximate incidence of metabolic disturbances associated with stone disease. Male veterans (n = 42), male non-veterans (n = 13), and women (n = 28) composed the group. We divided the groups in such fashion because they represented generally two distinct socioeconomic groups. Primary hyperparathyroidism was present in 19 per cent of the subjects; a marked predominance of women (15/16) was noted. Hypercalciuria of renal or intestinal origin was present in 23 per cent of the group. Of interest was a group of male veterans (17/83) in whom normocalciuria, normocalcemia, and normal serum phosphate were associated with high values of immunoreactive parathyroid hormone. These subjects had low urine phosphate. This set of findings indicates that these patients may be a new subgroup of stone-forming patients. Metabolic abnormalities could not be detected in 38 per cent of the patients. Classification of stone subjects is essential for rational management.

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