Developed End Stage Renal Failure Research Articles

IGA nephropathy: a retrospective evaluation of prognostic indices in 176 patients.

One hundred and seventy-six patients with mesangial IgA nephropathy have been studied retrospectively. Mean follow up from apparent onset of the disease was 9.3 years and with follow up from the diagnostic renal biopsy of 4.6 years. Our aim was to evaluate the prognostic significance of sex, age and type of symptoms at onset. The degree of proteinuria, presence of hypertension or decreased renal function, histological lesions and IFL pattern at the time of the diagnostic renal biopsy were recorded. 17 of the patients developed End Stage Renal Failure (ESRF) during the study. According to the Logrank test (renal survival) and Cox stepwise proportional hazard model, severity of glomerular mesangial lesions and degree of proteinuria are the most important indicators of a poor prognosis. The significance of all other parameters disappear after correction for histological lesions and degree of proteinuria. Our conclusion is that a semiquantitative light microscopical examination is an excellent prognostic index in IgA nephropathy, as is a simple determination of protein excretion in the urine.

Proteinuria in IgA nephropathy

Clinicopathological data in 74 patients with IgA nephropathy were analyzed with special attention to level of proteinuria and its prognostic significance in this disease. Excretion rates exceeding 3 g per day (heavy), in the range of 1 to 2.9 g (moderate) and under 1 g per day (mild) each occurred in approximately equal proportions of patients. One-sixth of those with more than 1 g developed end-stage renal failure, while serum creatinine never exceeded 2 mg/dl in any with mild proteinuria. "Renal survival" (serum creatinine of 2 mg/dl or less) at five years after presentation was 100% in patients with persistently mild proteinuria, 87% in those whose protein excretion reached the moderate range, and 69% when heavy or nephrotic range proteinuria developed. Of significance, only rarely did mild proteinuria at presentation increase to higher levels. A correlation existed between level of protein excretion and severity of mesangial, segmental or global proliferation, glomerulosclerosis, podocyte effacement, interstitial infiltration, tubular atrophy and vascular sclerosis, even in patients with unimpaired renal function. Moderate or heavy proteinuria typically preceded the onset of hypertension and occurred prior to the development of renal insufficiency. Our results underscore magnitude of proteinuria as an early marker of glomerular damage in the prognosis of IgA nephropathy.

Diabetics at end of queue.

Diabetics who develop end stage renal failure as a result of their condition tend to get put to the end of the queue when it comes to receiving treatment.

Long term prognosis of recurrent haematuria.

A long term follow up study of 100 children referred with recurrent haematuria for at least one year to two regional paediatric nephrology units is described. The mean duration of follow up was 8.2 years. An adequate renal biopsy was obtained in 96 and eight cases of Alport's syndrome and 10 of IgA nephropathy were diagnosed (20% and 26% respectively of the biopsies examined by electron microscopy and immunofluorescence). Five patients developed end stage renal failure and six hypertension requiring treatment, with the occurrence of these complications increasing progressively with increasing duration of follow up (1% at five years compared with 12% at 10 years). Adverse prognostic features were persistence of microscopic haematuria, proteinuria at presentation, and appreciable changes on renal biopsy. Eighty four patients had first degree relatives tested for haematuria; 30% of these families had another affected member. With long term follow up recurrent haematuria is associated with considerable morbidity and potential mortality.

Crescentic glomerulonephritis: immune vs. nonimmune mechanisms.

An immunopathological study of renal biopsies from 38 patients with glomerulonephritis with greater than 30% crescents was performed. All had evidence of immune deposits in glomeruli: 9 were characterized by linear fluorescence staining (antiglomerular basement membrane antibodies) and 29 had granular capillary wall and/or mesangial deposits. In the former group, 3 (33%) had associated pulmonary hemorrhage. In the latter group, the glomerular lesions in 18 (62%) were part of well-defined systemic illnesses, whereas in the remainder, the abnormalities were apparently limited to the kidney. The prognosis was uniformly grave, for all patients with adequate follow-up developed end-stage renal failure or died. In contrast to other reports of crescentic glomerulonephritis, we could not document the existence of an 'immunofluorescence negative' form of crescentic glomerulonephritis.

IgM associated primary diffuse mesangial proliferative glomerulonephritis.

Twenty-three cases of IgM associated primary diffuse mesangial proliferative glomerulonephritis are presented. In 18, IgM was the sole localising host immunoglobulin, and it was the predominant globulin in five; C3 was also present in 18. Light microscopy revealed variable diffuse and global mesangial proliferation in all cases, with additional focal global sclerosis in 16, focal segmental sclerosis in 15, and small capsular crescents in seven. Material for electron microscopy was available from 19 patients; in 13, occasional intramesangial electron dense deposits were identified, and in 18 there were irregular, rather ill defined areas of increased electron density in mesangial regions. Clinically, 14 patients presented with the nephrotic syndrome, and nine had asymptomatic proteinuria. During follow-up, only 10 patients showed no change in renal function or improved; the remainder showed increasing hypertension and/or renal function deterioration and four developed end stage renal failure. It is suggested that IgM associated mesangial proliferative glomerulonephritis should be considered as a distinct clinicoimmunopathological entity.

Prognostic importance of vascular lesions in acute renal failure with microangiopathic hemolytic anemia (hemolytic-uremic syndrome): Clinicopathologic study in 20 adults

Renal biopsies obtained from 20 adult patients within 30 days after onset of acute renal failure with microangiopathic hemolytic anemia ("the hemolytic-uremic syndrome") were studied. Lesions were graded independently by two observers without knowledge of the clinical history. All patients who did not have refractory hypertension were treated with heparin. Ten of the patients died, and four developed end-stage renal failure requiring chronic dialysis. Six patients, however, had a relatively good outcome: two recovered completely and four developed mild-to-moderate chronic renal failure not requiring dialysis. The six patients with a good outcome had significantly less severe arterial intimal thickening on biopsy compared with the remaining patients with a poor outcome. The patients with a good outcome and those with a poor outcome did not differ in the severity of glomerular lesions. The clinical features did not allow a prediction of late outcome. These results suggest that early renal biopsies may be helpful in predicting prognosis in the "hemolytic-uremic syndrome." This clinical syndrome may occur either in apparently healthy people, or may complicate the course of a chronic essential hypertension.

Malignant hypertension. Recovery of kidney function after renal allograft failure.

A 28-year old patient with malignant hypertension developed endstage renal failure necessitating chronic maintenance hemodialysis for seven months and transplantation of a renal allograft that was rejected within a month. After this, with continued control of the hypertension, the patient's own kidneys gradually resumed function and achieved anendogenous creatinine clearance of 30 ml/min. She has not required further dialysis for more than nine months. Recovery of sufficient renal function to maintain homeostasis, one year after onset of uremia, indicates the prolonged antihypertensive treatment period that may be necessary to reverse the renal arteriolar changes associated with malignant hypertension. This experience further underlines the necessity of moderation in the use of nephrectomy in the management of severe hypertension.

Current Status of Screening Children for Urinary Tract Infections

There is ample evidence that significant bacteriuria is frequent enough and procedures for mass screening are sufficiently developed to enable this country to mount a large scale program directed to the early detection of urinary tract infections. Information is now available on the epidemiology of bacteriuria, the frequency of associated structural abnormalities and methods to provide effective management. It is also clear that most female children with urinary tract infection generally will have a good prognosis. Few will develop endstage renal failure, but symptomatic infection is commonly associated with considerable morbidity. Unfortunately, it is not as yet possible to predict which child is at high risk of developing serious complications without searching for structural or neurologic abnormalities or by following individual patterns of recurrence. The ultimate impact on health and longevity is unknown even using data from the most structured programs. There is also the danger that mass programs may lead to false hope and eventual disillusionment if they are limited to detect infection and do not provide for further diagnostic, therapeutic and long-term follow-up of patients. For these reasons, urinary tract infection detection programs must be designed in relation to the realities of the current medical care system, the goals should be clearly defined and the expected result be stated honestly. AIMS OF THE PROGRAM There are two major reasons for screening children for urinary tract infection. One is to prevent the considerable morbidity from symptomatic infection and its complications so common in females throughout life. The other is to detect the population (often with anatomical abnormalities) at risk of developing pyelonephritis and subsequent renal damage.