To evaluate the influence of angiotensin II on kidney function in diabetic nephropathy we investigated the effect of angiotensin converting enzyme inhibition with captopril on glomerular filtration rate and albuminuria in hypertensive diabetics dependent on insulin and with persistent albuminuria.

Insulin action on kidney function was evaluated in 8 healthy subjects, (mean age 27 years) using the euglycaemic clamp technique. Insulin was infused at rates of 0, 20 and 40 mU.min-1.m-2 over consecutive periods of 120 min resulting in plasma insulin concentrations of 8 +/- 2, 29 +/- 7 and 66 +/- 14 mU/l. The renal clearance of 51Cr-EDTA, lithium, sodium and potassium was determined during the last 90 min of each period. Sodium clearance declined with increasing plasma insulin concentrations (1.3 +/- 0.4, 1.0 +/- 0.3 and 0.5 +/- 0.2 ml.min-1.1.73 m-2, p less than 0.001), while glomerular filtration rate (108 +/- 21, 104 +/- 21 and 108 +/- 20 ml.min-1. 1.73 m-2) and lithium clearance (a marker of fluid flow rate from the proximal tubules) 29 +/- 5, 29 +/- 4 and 30 +/- 4 ml.min-1.1.73 m-2) remained unchanged. Calculated proximal tubular reabsorption of sodium and water was unchanged, while calculated distal fractional sodium reabsorption increased (95.5 +/- 1.5, 96.4 +/- 1.2 and 98.1 +/- 0.7%, p less than 0.001). Potassium clearance and plasma potassium concentration declined, whereas plasma aldosterone and plasma renin concentrations were unchanged. In conclusion, elevation of plasma insulin concentration within the physiological range has a marked antinatriuretic action. This effect is located distally to the proximal renal tubules.

To diagnose fundic atrophic (type A) gastritis as part of the clinical investigation of various diseases or for epidemiologic purposes, a simple and reliable diagnostic test would be of great value. We studied circulating levels of pepsinogen A (PGA) and pepsinogen C (PGC) in 179 patients with fundic atrophic gastritis, 29 unselected patients with gastric adenocarcinoma, 15 totally gastrectomized patients, and 50 gastroscopically examined normal controls. Of 147 patients with severe atrophic gastritis, 42 (29%) had serum PGA and 22 (15%) serum PGC values within the range of those in totally gastrectomized patients. The most sensitive test for fundic atrophic gastritis was the PGA/PGC ratio in serum, the sensitivity and specificity being 99% and 94%, respectively (discrimination limit, 5.5). Correspondingly, the positive predictive value was 98%, and the negative predictive value 98%. Of 29 unselected patients with gastric adenocarcinoma 22 (76%) had serum PGA/PGC values lower than the discrimination limit for atrophic gastritis. We conclude that the relatively simple analysis of PGA and PGC in serum is a powerful test for fundic atrophic gastritis with several potential areas of application.