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Renal function was serially investigated during the development of hypertension in a 12.8-year-old girl with chronic glomerulonephritis. Clearances of inulin (CIn) and para-aminohippuric acid (CPAH), filtration fraction, and sodium excretion were measured during hydropenia and isotonic saline volume expansion. Blood pressure was initially labile, but after a few years fixed hypertension developed, and antihypertensive treatment with propranolol was started. During the early stages of hypertension, the filtration fraction during hydropenia was reduced, but the natriuresis during volume expansion was normal. When the hypertension was fixed, glomerular filtration rate, CPAH, and filtration fraction were normal, but the natriuresis was exaggerated. Antihypertensive treatment only partially corrected the natriuresis.

Renal function was studied in three patients with post-streptococcal, four patients with IgA and one patient with non-streptococcal proliferative glomerulonephritis (GN) at the onset of the disease and two, six and 12 months later. Renal biopsies were performed at the onset of the disease and 12 months later. Standard clearance techniques were used for the functional studies. The latter were performed during hydropenia and continuous isotonic saline infusion. During hydropenia, the GFR was uniformly depressed shortly after the onset of the disease, but it normalized during the following two months. The filtration fraction was depressed in poststreptococcal GN at the onset and it normalized with the GFR. In IgA GN, the filtration fraction remained within normal limits during the entire course of the illness. The natriuretic response to isotonic saline volume expansion was low in all patients at the onset of the disease, but normalized in post-streptococcal and IgA GN during the one-year follow-up. In spite of normalized renal function, biopsy findings in IgA GN were unchanged 12 months later. An episode of macroscopic hematuria in one patient with IgA GN at the six-month investigation had no apparent effect on renal function.

The pathophysiology of IgA GN was investigated in different stages of the disease. Seventeen patients who were between 3.5 and 16.5 years of age at the onset were included in the study. Clearance studies were performed repeatedly in 6 patients (in 5 of them over a period extending from the onset to 5-9.5 years) and only once in 9 patients (10-23 years after the onset). Two patients (one with uremia) were only evaluated clinically. CIn, CPAH and UNaV were studied during hydropenia (HP) and 3% isotonic saline volume expansion (VE). Shortly after the onset CIn, CPAH and UNaV were depressed. Renal function was essentially normal and 1 and 2 years after the onset in spite of signs of active disease. A supernormal GFR was found in 7 patients after they had had the condition between 5 and 17 years. After a duration of IgA GN for greater than 9 years 3 of 12 patients had developed hypertension and uremia and 2 had hypertension or labile BP. Three of 10 patients had a normal GFR and BP, but had increased natriuresis during VE. Only 2 of 10 patients were normotensive and had normal renal function. Disturbances in the renal function are thus frequent in all stages of IgA GN and the changes seem to be related to the duration of the disease. Exaggerated natriuresis may indicate progressive disease.

Thirteen patients with active IgA glomerulonephritis (IgA GN), ten patients with a history of Henoch-Schönlein glomerulonephritis (HS GN) and nine healthy controls were studied during hydropenia (HP) and 3% volume expansion (VE) with isotonic saline. Clearance of inulin and para-aminohippurate, urinary excretion of Na, immunoreactive prostaglandin F2 alpha (PGF2 alpha) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were determined. The patients with a history of HS GN had normal blood pressure and renal function. As in the controls, the urinary excretion of PGF 2 alpha decreased and the excretion of 6-keto-PGF1 alpha increased during VE. In the patients with IgA GN the glomerular filtration rate (GFR) was normal, markedly reduced and supernormal. Five patients had hypertension and an increased NA excretion in relation to the GFR during VE. As a group, the patients with IgA GN increased their urinary excretion of 6-keto-PGF1 alpha during VE, while the excretion of PGF2 alpha did not change. In relation to the GFR, the urinary excretion of PGF2 alpha and 6-keto-PGF1 alpha was markedly increased in two patients with low GFR, which implies that these substances play a role in advanced renal disease. VE had little effect on PG excretion in these patients. In the hypertensive patients the urinary excretion of PGF2 alpha and 6-keto-PGF1 alpha was the same as in those with normal blood pressure. PGs are therefore not likely to mediate the increased natriuretic response to VE in hypertension.

Renal function studies were performed in 18 subjects in different stages of Henoch-Schönlein glomerulonephritis (HS GN). Nine children were serially investigated, and nine adolescents or young adults, who were considered to have clinically recovered, were investigated only once, 10.5-14 years after the onset. Inulin and PAH clearance, as well as sodium excretion, were determined during hydropenia (HP) and 3% volume expansion (VE) with isotonic saline. In most patients in the former group a renal biopsy was performed during the first investigation and again one year later. The early disturbances in renal function resembled those we have found in other types of GN. The GFR was normal during HP or after VE in most cases one year after the onset. The natriuretic response to VE was decreased in most patients initially, and this was found to persist in half of the patients 2-3 years after the onset. Pathological urinalyses then indicated disturbances in the renal handling of sodium. A reduced capacity to excrete sodium, however, did not seem to be of prognostic significance since all patients, except one who developed renal insufficiency and hypertension, had normal urinalyses and blood pressure six years after the onset. This study provides no evidence that subjects with previous HS GN will later develop impaired renal function or be predisposed to hypertension.