In order to assess the ability of the diseased kidney (DK) to modulate renin output in response to extracellular fluid (ECF) volume expansion and intravenous furosemide administration, we studied eight dogs with experimentally induced, unilateral pyelonephritis. The contralateral normal kidney (CK) maintained a nonazotemic environment, thereby removing the multiple variables associated with azotemia from the specific consequences of intrinsic renal disease. Measurement of renal vein plasma renin activity, glomerular filtration rate (GFR) and total renal plasma flow showed that baseline renal vein renin output in relation to GFR was similar in DK and CK. Following acute ECF volume expansion, renin output by DK was suppressed to the same degree as CK. Intravenous furosemide administration elicited increments in renal vein plasma renin activity from DK and CK which were not significantly different. The data suggest that residual nephrons of the chronically diseased kidney maintain integrity of their endocrine function, in addition to integrity of many excretory and metabolic functions as documented by previous studies.