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Extract: The growth of children with chronic renal disease is poor and the cause of this stunting is not known. Various factors have ben implicated and it is difficult to evaluate their relative importance in clinical studies. Accordingly, there is a need for an animal model, preferably one which enables the effect on growth of a number of factors to be studied separately and over a reasonably short period of time. The growth and food intake of male and female rats rendered uremic by 5/6 nephrectomy was observed between 40 and 70 days of age for male rats and between 35 and 70 days of age for female rats. Final mean body weight for males with uremia (243 g ± 32 g) was significantly less than for control males (323 g ± 24 g); final mean body weights for female rats were also significantly different (172 g ± 17 g; 223 g ± 21 g). The differences in body weight were apparent from 50 days onwards. Final tail length was significantly less in female uremic rats compared with their control subjects (173 mm ± 8 mm; 183 mm ± 7 mm). Uremic rats matched for body weight with control rats consumed significantly fewer calories; for both groups the average difference was about 15%. Multiple regression analysis of weight gain against age and calorie intake suggests that there may be an increase in the calorie cost of growth in rats with uremia, but these findings require confirmation in paired feeding studies. Speculation: These studies suggest that this rat model can be used for the investigation of alterations in energy balance, body composition, and metabolic functions in uremia. It should be possible to study the effects of single variables in the pathogenesis of growth retardation by appropriate manipulations halfway through the growth period.

Fifty-eight children with minimal-change nephrotic lesions who relapsed repeatedly and showed toxic side effects from corticosteroids were treated with cyclophosphamide for an average of 12 weeks. The initial dose was 5 mg/kg/day. Four to seven years (mean 5.8 years) later 20 remained in remission, 34 were still relapsing, and 4 had died (two during relapses, one of measles after cyclophosphamide, and one of a brain-stem astrocytoma). The half time for the relapse-free period after treatment was 2.8 years. There was no relationship between the length of treatment with cyclophosphamide and the stability of remission within the limits studied.

Fifteen patients with rapidly progressive glomerulonephritis (R.P.G.N.) were treated with quadruple chemotherapy—i.e., prednisolone, azathioprine or cyclophosphamide, dipyridamole, and heparin followed by warfarin. In addition, one patient was treated with anticoagulants and dipyridamole only. The diagnosis of R.P.G.N. was based on a clinical course with rapidly deteriorating renal function in patients in whom occluding extra-capillary crescents were present in more than 60 of glomeruli in an adequate renal-biopsy specimen Of these sixteen patients, six had idiopathic R.P.G.N. (of whom three had mesangiocapillary glomerulonephritis), four had systemic lupus erythematosus, two had polyarteritis nodosa, two had Henoch-Schonlein purpura, one had relapsing polychrondritis, and one had post-streptococcal glomerulonephritis. These patients were treated for periods of 1 to 34 months. Six had oligo-anuria at the start of therapy and the remaining ten had glomerular-filtration rates between 3·2 and 21·6 ml. per minute. None of those who were oligo-anuric responded to this form of therapy, but renal function improved in all those with progressive renal failure, irrespective of the clinicopathological diagnosis. Two patients had moderate gastrointestinal bleeding and heparin was stopped; in one bonemarrow activity was suppressed by azathioprine. There were no serious consequences in any of these patients.

As part of a larger study of serial complement profiles in glomerulonephritis plasma C3 and C4 concentrations were measured using commercially available immunodiffusion plates. A total of 303 samples were obtained from 128 patients suffering from forms of nephritis associated with hypocomplementaemia-namely, lupus nephritis, mesangiocapillary glomerulonephritis (M.C.G.N.), and acute glomerulonephritis.These simple measurements of C3 and C4 gave clinically useful information. In lupus nephritis C3 and C4 generally correlated and C4 concentrations were more often and more profoundly depressed than C3 concentrations. Neither C3 nor C4 concentrations alone correlated well with the antinuclear factor titre.In both acute glomerulonephritis and M.C.G.N. the C3 concentrations were frequently lower than 20% of normal (which was never the case in patients with lupus), while the C4 concentration was usually normal and was almost never depressed in the absence of C3 depression. This suggests activation of complement at the C3 level by the "bypass" pathway in acute nephritis as well as in M.C.G.N., though both may be operating in some patients. In acute glomerulonephritis but not in M.C.G.N. C3 concentrations returned to normal within eight to 12 weeks.The two varieties of M.C.G.N. identified by the site of the deposits in the capillary glomerular walls differed in their C3 levels. In 10 patients with intramembranous dense linear deposits the C3 was always low over very long periods of time, rising in three out of four patients only after transplantation and immunosuppression. Other patients with M.C.G.N., in contrast, often showed normal C3 concentrations. Concentrations of C4 did not differ in either group, being normal in 80% of samples from all types.

Renal puncture was used in the diagnosis of five infants with suspected cystic disease of the kidney. This technique is simple and it may provide information that may otherwise be difficult to obtain.