The changing natural history of nephropathy in type I diabetes

Events in the natural history of diabetic nephropathy (including the onset of persistent proteinuria and end-stage renal failure) were studied in a cohort of 292 patients with juvenile-onset type I diabetes who were followed for 20 to 40 years. The risk of persistent proteinuria increased rapidly between the fifth and 15th years of diabetes and declined thereafter. This pattern suggests that susceptibility to this complication was limited to a subset of patients and was exhausted over time. Patients with the most frequent severe hyperglycemia (the highest quartile) during the first 15 years of diabetes had a risk of persistent proteinuria that was four and a half times higher than that for those with the least frequent hyperglycemia (the lowest quartile). Patients whose diabetes was diagnosed in the 1930s had twice the risk of persistent proteinuria as those in whom the condition was diagnosed in later decades. Once persistent proteinuria appeared, progression to renal failure almost always followed. Half reached this stage within 10 years, and the interval for progression did not vary according to sex, frequency of hyperglycemia, or calendar year of diagnosis of diabetes. This period, however, was significantly shorter (eight versus 14 years) for patients whose diabetes was diagnosed after puberty than for those who were younger at onset. In conclusion, the development of diabetic nephropathy consists of at least two stages. The onset of proteinuria, although related to the level of exposure to hyperglycemia, appears to be influenced by genetic and/or environmental factors. The second stage, progression to renal failure, seems to be influenced by processes related to maturation or aging.     

Chronic renal failure in non-insulin-dependent diabetes mellitus. A population-based study in Rochester, Minnesota

STUDY OBJECTIVE: To identify the incidence of clinically defined chronic renal failure by clinical type of diabetes in a community diabetic incidence cohort, and to evaluate the relation between persistent proteinuria and chronic renal failure in non-insulin-dependent diabetes mellitus. DESIGN: Retrospective incidence cohort study. SETTING: Population-based in Rochester, Minnesota. PATIENTS: Residents of Rochester, Minnesota, with diabetes initially diagnosed between 1945 and 1979 who had follow-up to 1984 for clinically defined chronic renal failure. MEASUREMENTS AND MAIN RESULTS: Among 1832 persons with non-insulin-dependent diabetes who were initially free of chronic renal failure, 25 developed chronic renal failure (incidence, 133 per 100,000 person-years: CI, 86 to 196). The subsequent incidence of chronic renal failure among 136 insulin-dependent diabetic Rochester residents, three of whom developed chronic renal failure, was 170 per 100,000 person-years (CI, 35 to 497). After adjusting for potential confounding factors, we found that the risk for chronic renal failure associated with the presence of persistent proteinuria at the time of the diagnosis of non-insulin-dependent diabetes was increased 12-fold (hazard ratio, 12.1; CI, 4.3 to 34.0). When persistent proteinuria developed after the diagnosis of non-insulin-dependent diabetes mellitus, the cumulative risk for chronic renal failure 10 years after the diagnosis of persistent proteinuria was 11%. CONCLUSIONS: These population-based data suggest that most cases of chronic renal failure in diabetes occur in persons with non-insulin-dependent diabetes. These data also identify the increased risk for chronic renal failure among persons with non-insulin-dependent diabetes mellitus who have persistent proteinuria present at or developing after the diagnosis of non-insulin-dependent diabetes mellitus, such data may be useful for directing interventions to prevent or delay the development of chronic renal failure.     

IgA nephropathy: frequent, but rarely diagnosed

IgA nephropathy (IgAN) is the most common type of glomerulonephritis in the western world. In the majority of cases, it manifests in adolescence or early adulthood as recurrent macrohematuria, frequently triggered by infections, or persistent microhematuria as well as mild proteinuria, hypertension and/or renal insufficiency. In view of the later, it is not surprising that IgAN is often a chance finding. The majority of affected persons probably never come to medical attention, since in autopsies a prevalence of up to 1% of the population has been reported. About 20-30% of patients with a diagnosis of IgAN suffer from chronic, slowly progressive renal failure. Predictors include the degree of proteinuria and arterial hypertension as well as the established renal impairment at the time of diagnosis. Early identification of this risk group is of particular importance, since adequate therapy can stop or at least retard the progression of renal failure. When end stage renal failure has developed and a renal transplant is performed, about 25% of the patients will experience a clinically relevant recurrence of IgAN with progressive graft dysfunction.     

Changing profiles of proteinuria in renal transplantation. Predictive factors for its appearance

Proteinuria is a risks factor that accelerates the progression of renal insufficiency by several mechanisms. In the renal transplant proteinuria is a predictor of progressive renal insufficiency and it is associated with poor patient and graft survival. We have performed a longitudinal observational case-control study to defect and quantify proteinuria in a group of 100 cadaveric renal transplant recipients and to evaluate the influence of several factors on its appearance. We have considered the variables age and sex of the donor and recipient, number of HLA-DR, A and B mismatches, cold ischemia time, basal renal disease, initial immunosuppression, immediate versus delayed graft function and acute rejection. Three patients who did with a functioning graft were excluded from the analysis of the data. All variables were analysed in a regression model of multivariate analysis. Proteinuria in the moths 1, 3, 6, 9 and 12 was: 0.38 +/- 0.27 g/day, 0.38 +/- 0.32 g/day, 0.44 +/- 0.99 g/day, 0.42 +/- 0.58 g/day and 0.37 +/- 0.54 g/day, respectively. We analysed the profile of the proteinuria in each patient individually. Fifty three patients (54.6%) did not develop proteinuria, 12 patients (12.4%) had transient initial proteinuria, 23 patients (23.7%) had persistent proteinuria and 9 patients (9.3%) had progressive proteinuria. The renal function differed between groups. Higher creatinine levels were found in the patients with persistent proteinuria and those with progressive proteinuria. We analysed the patients according to several variables. The age of the donor was higher in the group of patients with persistent proteinuria and the incidence of acute rejection was higher in the group of patients who developed progressive proteinuria, with differences statistically significant. There was no difference in the univariate analysis in the other variables considered. The multivariate analysis confirms that the age of the donor and the basal glomerular disease predict persistent proteinuria and acute rejection predicts progressive proteinuria. According to our study, proteinuria is frequent in the renal transplant recipient with different evolutionary profiles. Two types are associated with bad renal function and have different predictive factors. We encourage the use of drugs which reduce proteinuria.     

Continued absence of clinical renal disease seven to 12 years after poststreptococcal acute glomerulonephritis in Trinidad.

Continued improvement was noted among 722 patients in Trinidad seven to 12 years after the onset of poststreptococcal glomerulonephritis. In the five years since earlier follow-up, two of 709 patients with previous symptomatic disease apparently had died from renal failure, and 10 patients had died from unrelated causes. Nineteen patients presently had proteinuria, three had hematuria, and three had proteinuria plus hematuria. Of these abnormalities, proteinurias in only three patients and proteinuria plus hematurias in three more patients were persistent. Thus, 0.8 per cent of the study group had persistent abnormalities. When one adds those dead with renal disease, the percentage with renal damage becomes 1.1 per cent. In addition, six patients had protein in the two urine samples obtained after assuming the lordotic position for 10 minutes and in only one of the two urine samples obtained upon rising in the morning, making 1.4 per cent with probable evidence of chronic renal disease, including the dead patients. Hypertension was present in 16 (2.3 per cent) of the patients and was much more common in those more than 20 years old (18.4 per cent). However, this prevalence of hypertension did not exceed that found in normal Trinidadians. Only three patients had serum creatinine values greater than 1.2 mg/dl. None of 13 patients with previous asymptomatic glomerulonephritis presently showed any abnormality. Thus, very few cases of chronic poststreptococcal glomerulonephritis appear to have developed in the 722 patients studied.     

Urinary Tract and Renal Findings in Acute Yersinia Infections

ABSTRACT We studied 71 patients with acute Yersinia infection for the occurrence of pathologic urinary and renal findings. Transient proteinuria and/or microhematuria was found in 17 patients (24%) and slightly elevated serum creatinine in seven patients (10%). Renal biopsy was done in two patients and revealed mild mesangial glomerulonephritis in both cases. One of these patients had IgA glomerulonephritis and Reiter's syndrome. Pyuria occurred in 16 patients (23%) and was frequently associated with Reiter's syndrome. Seventy-three patients with acute intrinsic renal failure were studied for the occurrence of acute Yersinia infection by determining Yersinia antibodies by ELISA. One out of 13 patients with acute glomerulonephritis but none of 60 patients with acute tubulointerstitial renal disease had acute Yersinia infection. Acute Yersinia infection seems to be rarely an etiologic factor in acute intrinsic renal failure. Our results indicate that transient proteinuria, microhematuria, pyuria or impaired renal function are frequent findings in patients with acute Yersinia infections. However, glomerulonephritis seems to be a rather infrequent and mild complication of acute Yersinia infection.     

Proteinuria: potential causes and approach to evaluation

Proteinuria may be associated with a renal or systemic disease, or it may be isolated. The latter occurs in asymptomatic patients without evidence of any disease or abnormality of the urine sediment. Isolated proteinuria may be subdivided into two broad groups: (1) benign forms, with a favorable-to-excellent prognosis and (2) persistent forms, some of which have a worrisome prognosis. Functional proteinuria may occur in disorders with altered renal hemodynamics, usually resolves, and is not associated with progressive renal disease. Idiopathic transient proteinuria is typically discovered on routine screening and usually disappears on subsequent testing. In idiopathic intermittent proteinuria, a significant number (50%) of urine samples exhibit abnormal rates of protein excretion. Although structural abnormalities may be observed on renal biopsy, progressive renal insufficiency is unusual. In orthostatic proteinuria, the rate of protein excretion completely normalizes in the recumbent position. Long-term studies show this to be a benign condition. In persistent isolated proteinuria, at least 80% of random urine samples exhibit abnormal protein excretion. This represents a heterogeneous group, but a significant proportion of these patients have prominent renal pathologic findings and progress to serious renal disease. Proteinuria with significant renal disease may be non-nephrotic or nephrotic range. The former does not exclude glomerular disease, but tubulointerstitial or vascular disorders are also likely when proteinuria is less than 2 g/24 hours. Patients with nephrotic-range proteinuria generally have a glomerular disorder. Distinction between benign and more ominous forms of proteinuria requires careful evaluation.     

IgA-Nephropathie

IgA nephropathy (IgAN) is the most common type of glomerulonephritis in the western world. It usually manifests in young adulthood as an oligosymptomatic disease with recurrent episodes of macrohematuria or persistent microhematuria, mild proteinuria and/or renal failure. Thus, it is not surprising that IgAN is usually a chance finding and would probably never have been discovered in many of those affected. About 20% of the diagnosed patients experience chronic progressive renal failure. Predictors are the extent of proteinuria, hypertension as well as already manifested renal failure at the time of diagnosis. Early identification of this risk group is of eminent importance as an optimal supportive therapy can arrest or at least reduce progression of renal failure. The value of immunosuppressive therapy is comparably less well established, so that it should be reserved for those patients maintaining a high proteinuria or losing renal function despite optimized supportive care.     

Berger's disease in children. Natural history and outcome

The clinical course and outcome of 91 children less than 15 years of age at onset and followed for at least 1 year have been retrospectively analyzed. The course has been characterized by recurrent macroscopic hematuria in 74 patients, by proteinuria-microscopic hematuria and a single episode of macroscopic hematuria occurring either at onset or a few months later in 8, by proteinuria-microscopic hematuria in 7, and by proteinuria only in 1. Lastly, one patient showed rapidly progressive renal failure. Four groups were identified by light microscopy: minimal glomerular changes (26), focal and segmental glomerulonephritis (41), pure mesangial proliferation (3) and proliferative glomerulonephritis with crescents (21). A good correlation was found between the glomerular lesions observed by light microscopy and the outcome. In this series we have not observed a dramatic clinical deterioration suggesting a transformation from one histologic type to another, as reported by others. None of the 70 patients belonging to the first three groups has impaired renal function but two with focal and segmental glomerulonephritis have developed hypertension. Although the clinical course is benign, many patients have, at the last observation, an abnormal urinalysis characterized by microscopic hematuria and/or mild proteinuria; the proteinuria is over 1 g/24 h in six patients with focal and segmental glomerulonephritis. Ten patients remained in clinical remission for several years, but mesangial IgA deposits were still present in the only patient who had a repeat biopsy while in remission. In contrast, none of the patients with proliferative glomerulonephritis with crescents has had a prolonged remission. Six patients developed terminal renal failure 0.7, 0.11, 2, 4, 8 and 10 years after onset. Two additional patients are in moderate chronic renal failure with hypertension 10 and 12 years after onset. Most children show a persistent nephropathy, (in five proteinuria is over 1 g/24 h), and two of them have developed hypertension. Therapeutic trials using drugs with side-effects should, therefore, be used only in this group of patients.     

Angiotensin inhibition or blockade for the treatment of patients with quiescent lupus nephritis and persistent proteinuria

Angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor blocker (ARB) reduces proteinuria and the rate of renal function deterioration in diabetic nephropathy and other glomerular diseases, but its role in quiescent lupus nephritis has not been established. We conducted a retrospective study to investigate the effects of ACEI/ARB on proteinuria and renal function in patients with persistent proteinuria (>1 g/day) despite resolution of acute lupus nephritis following immunosuppressive treatment. Fourteen out of 92 patients were included. The duration of treatment with ACEI/ARB was 52.1 +/- 35.7 months. The levels of proteinuria, serum albumin, serum creatinine, systolic and diastolic blood pressure were 1.10 to 6.90 g/day, 35.8 +/- 3.6 g/L, 102.54 +/- 34.48 micromol/L, 137.6 +/- 10.9 and 81.9 +/- 9.2 mmHg at baseline. Proteinuria and serum albumin showed significant sustained improvements after 6 and 24 months of treatment. Comparison of slopes for serial proteinuria, albumin and reciprocal of serum creatinine before and after treatment showed significant improvements in six (43%), eight (57%) and two patients, respectively. At last follow-up proteinuria remained significantly lower (0.36 g/day, P = 0.043) and albumin higher (41.3 +/- 2.2 g/L, P = 0.023). Eleven (78.6%) patients had proteinuria improved by >50%, and five had insignificant proteinuria at last follow-up. Systolic blood pressure was significantly reduced from 6 months onwards, but this did not correlate with proteinuria reduction. Diastolic blood pressure, serum creatinine, creatinine clearance, anti-dsDNA, C3 and haemoglobin were not altered. We conclude that ACEI/ARB effectively reduces proteinuria and improves serum albumin in patients with persistent proteinuria despite quiescent lupus nephritis.     

Diabetic renal disease in central Africa

Six hundred African diabetic patients were examined using a protocol based on the WHO Multinational study in which no country from Africa was represented. The salicylsulphonic acid test for proteinuria was used to assess the presence of diabetic renal disease. Overall 23.8% of patients had proteinuria (95% confidence interval 20.4 to 27.2) and 3.8% chronic renal failure (95% confidence interval 2.3 to 5.3). Patients with proteinuria were older and had had diabetes longer than those without (p less than 0.001). Systolic blood pressure rose with increasing proteinuria in both sexes but only men with severe nephropathy showed an increase in diastolic pressure. Minimal diabetic nephropathy was more common than severe nephropathy which carried a particularly poor prognosis in African diabetic patients due to lack of resources.     

Familial factors determine the development of diabetic nephropathy in patients with IDDM

Summary To evaluate familial factors in the development of diabetic nephropathy in insulin-dependent diabetes mellitus (IDDM) we examined concordance for diabetic nephropathy in families with multiple IDDM siblings. Families (n=110) were identified through Joslin Clinic patients (probands) with a sibling having IDDM. To be eligible, the probands' and siblings' ages at IDDM diagnosis were less than 21 years, and IDDM duration was more than 15 years for probands and more than 10 years for siblings. Mean post-pubertal diabetes duration was 23 years for probands (n=110) and 21 years for siblings (n=125). Nephropathy history was determined by medical record review for deceased patients and those with persistent proteinuria or end-stage renal disease to ascertain the date of onset of persistent proteinuria. For patients without documented nephropathy, the albumin/creatinine ratio was measured in multiple urine samples. The cumulative incidence of persistent proteinuria according to post-pubertal duration of IDDM was determined by life-table analysis. For probands and siblings combined, the cumulative incidence of advanced diabetic nephropathy after 30 years of IDDM was 35%, but the risk in siblings varied according to the proband's renal status. The cumulative risk in siblings after 25 years of IDDM (post-puberty) was 71.5% if the proband had persistent proteinuria but only 25.4% if the proband did not (p<0.001). A difference of nearly 50% in the risk to IDDM siblings, depending upon the IDDM proband's renal status, is consistent with a major gene effect that predisposes an individual with IDDM to develop advanced diabetic nephropathy.Abbreviations IDDM Insulin-dependent diabetes mellitus - C.I. confidence interval     

Renal biopsy in lupus patients with low levels of proteinuria

OBJECTIVE: Early and accurate detection of kidney involvement in systemic lupus erythematosus (SLE) improves outcomes. Renal biopsy is required for definitive diagnosis of lupus nephritis (LN). In the absence of acute renal failure (ARF), moderate levels of proteinuria (> 1000 mg/24 h) have been recommended by some to justify biopsy. We investigated whether patients with lower levels of proteinuria without ARF have significant renal disease and should be routinely biopsied. METHODS: We retrospectively evaluated 21 SLE patients with 24-h urine protein < 1000 mg who underwent kidney biopsies. Indications for biopsy included new-onset proteinuria, increasing proteinuria, or hematuria (> 5 red blood cells per high power field). No patient had ARF. RESULTS: Sixteen of 21 (77%) biopsies were diagnostic of LN: 3 class II, 10 class III (5 superimposed class V), 2 class IV (one superimposed class V), and one with class V. One patient had thrombotic microangiopathy. The remaining 4 (23%) patients had non-lupus renal disease. Thirteen patients with class III or greater LN required alterations in therapeutic regimen because of biopsy findings. Of 7 patients without hematuria at the time of biopsy, 4 (57%) had class III, IV, or V LN. One patient without hematuria and < 500 mg/24 h proteinuria had class III LN. CONCLUSION: We found significant renal involvement (Class III, IV, or V LN) in SLE patients with < 1000 mg proteinuria with or without hematuria. Our findings suggest that biopsy be strongly considered in this patient population.     

A community-based study of chronic kidney disease among type 2 diabetics in Kinmen, Taiwan

Diabetic nephropathy is the major cause of end-stage renal disease. Many studies show that chronic kidney disease can be prevented, or its progression to end-stage renal disease delayed, by effective intervention. The aim of this study was to estimate the prevalence of proteinuria and renal impairment in patients with type 2 diabetes. A community-based screening for chronic kidney disease in type 2 diabetic patients was conducted in 1999-2001. Proteinuria was defined in terms of urine protein-to-creatinine ratio. The glomerular filtration rate per 1.73m(2) body surface area was calculated using an equation from the Modification of Diet in Renal Disease Study. The overall response rate was about 78.6%. Prevalence rates of proteinuria and renal impairment were 29.4% and 15.1%, respectively. Females had higher prevalence of proteinuria and renal impairment than males. And prevalence increased with increasing age. Hypertension was associated with both proteinuria and renal impairment. Only 43.0% of patients with stages 3-5 chronic kidney disease had proteinuria. Proteinuria and renal impairment screening may identify different segments of the diabetic population. Both a glomerular filtration rate and proteinuria test are recommended as screening tools for early detection of chronic kidney disease in type 2 diabetics.     

Effect of race on expression of acquired immunodeficiency syndrome-associated nephropathy

The prevalence of renal disease associated with the acquired immunodeficiency syndrome (AIDS) is unknown, but appears to vary in different regions. Centers in New York, NY, and Miami, Fla, have reported patients with renal disease complicating AIDS. These populations have included large proportions of black patients and intravenous drug abusers. Reports from San Francisco, Calif, have suggested the prevalence of renal disease complicating AIDS is low, but the population was composed primarily of white patients, with a low proportion of drug abusers. The George Washington University Medical Center was the site of treatment for 31.4% of the patients with AIDS in Washington, DC. This population was split roughly evenly between black and white patients. A retrospective survey of patients with both AIDS and renal disease revealed approximately two thirds of the patients were black, reflecting the demographics of the population with AIDS; 11% of patients had intravenous drug abuse as a risk factor for the development of AIDS; and 74% had acute renal failure. Of these patients, approximately equal proportions were black and white. Twenty-six percent of the population had chronic renal failure, but the overwhelming proportion were black. There were no differences between proportions of patients in age, sex, race, or risk factors in patients with acute renal failure and chronic renal failure, but there was a significant difference in the proportions of black and white patients with chronic renal failure. The reason for these differences is unknown, but differences in host responses to viral proteins, physiologic adaptations, or socioeconomic factors in these populations may play an important role in mediating the expression of renal disease in individual patients.     

Optimal nephroprotection: Use,misuse and misconceptions about blockade of the renin–angiotensin system. Lessons from the ONTARGET and other recent trials

Results from the ONTARGET trial remind us that acute haemodynamically mediated renal dysfunction, triggered by low arterial pressure or volume depletion, can occur in high-risk cardiovascular patients (who usually have some degree of diseased intrarenal vessels) treated with renin–angiotensin system (RAS) blockers (especially in combination). However, nephroprotection could not be properly assessed in the trial, as the population was at low renal risk. Although albuminuria remains a useful marker in many patients, it can neither predict acute renal dysfunction nor replace end-stage renal disease (ESRD) as the endpoint in clinical trials. Recent trials using surrogate endpoints suggest that some RAS blockers (ACE inhibitors, angiotensin receptor blockers, the renin inhibitor aliskiren) may be more nephroprotective than others, but proving this requires comparing them (alone or in combination) in populations with identified renal disease (mainly diabetic nephropathy) and the use of hard endpoints. RAS-blocker dosages are critical: as some patients need much larger doses to decrease proteinuria than do others, the efficacy of a high-dose RAS blocker needs to be assessed in patients with persistent proteinuria. In patients with massive proteinuria despite maximum RAS-blocker dosages, combination RAS blockade should be considered by nephrologists, but will require close monitoring of renal function; also, the treatment needs to be withdrawn (at least temporarily) as soon as volume depletion or excessively low arterial pressure arises. In recent trials, lowering blood pressure towards values recommended by the current guidelines (130/80 mmHg) has reduced microvascular (lower levels of urinary albumin excretion) and macrovascular events in diabetic patients.     

Clinical features and long-term outcome of 91 cases of adult onset post-streptococcal glomerulonephritis in Hong Kong

The clinical features and long-term outcome of 91 cases of adult-onset PSGN in Hong Kong were reported. There were 46 male and 45 female with age ranging from 13 to 56 yrs (mean 18.6). The diagnosis was based on clinical manifestations and renal biopsy was performed in 29 cases. The main manifestations were acute nephritic syndrome (72.5%) and acute nephritic-nephrotic syndrome (27.5%). Serum creatinine was increased in 48.4% of the patients at presentation. Four cases presented with acute renal failure. Serial serum C3 levels were determined in 48 patients. It was decreased in all patients at presentation but returned to normal within 15 weeks. The follow-up duration of this series ranged from I to 19 yrs (mean 4.73 yr) 67.03% recovered early (within 3 mts); 14.29% recovered later (from 6 mts to 7 yrs): 16.48% had persistent or intermittent proteinuria and or haematuria. Two cases developed chronic renal insufficiency. Our results suggested that the prognosis of PSGN in adults is relatively good and the indications for renal biopsy in adult-onset PSGN were discussed.     

Proteinuria should be used as a surrogate in CKD

Surrogate end points of renal failure are instrumental to the testing of new treatments in patients with chronic kidney disease, the natural history of which is characterized by a slow, asymptomatic decline in renal function. The magnitude of proteinuria is widely recognized as a marker of the severity of glomerulopathy. Population-based studies have identified proteinuria as a predictor of future decline in glomerular filtration rate and of the development of end-stage renal disease. More importantly, a reduction in proteinuria invariably translates into a protection from renal function decline in patients with diabetic and nondiabetic renal disease with overt proteinuria. Thus, proteinuria should be considered a valuable surrogate end point for clinical trials in patients with proteinuric renal diseases.     

Cardiac hypertrophy in diabetic nephropathy: an echocardiographic study

Echocardiography was used to study the prevalence and severity of left ventricular hypertrophy in patients with established diabetic nephropathy (persistent proteinuria for at least 2 y plus severe retinopathy). Fifteen patients had mild renal impairment (serum creatinine less than 150 mumol l-1), 14 patients had moderate renal impairment (serum creatinine 150-400 mumol l-1), and 20 patients had severe renal impairment (serum creatinine greater than 400 mumol l-1). Thirty-six of the 49 (73%) were on anti-hypertensive treatment, despite which mean blood pressure was 161 +/- 25/89 +/- 9 (+/- SD) mmHg. Left ventricular hypertrophy was demonstrated in 42 of the 49 patients (85%), and increased in severity with increasing renal impairment. Interventricular septal + left ventricular posterior wall thickness was 25 +/- 3 mm in those with mild renal impairment, 28 +/- 6 mm in those with moderate renal impairment and 30 +/- 4 mm in those with severe renal impairment. The most severe left ventricular hypertrophy was seen in the Afro-Caribbean patients. Left ventricular hypertrophy was present even in those with marginally raised blood pressure and was related to age and serum creatinine but not to present blood pressure or duration of proteinuria.     

Proteinuria in benign nephrosclerosis

Benign nephrosclerosis seldom is associated with significant proteinuria or reduced renal function. This study demonstrated that, despite the finding of benign nephrosclerosis on a renal biopsy specimen, concomitant proteinuria is predictive of a poor prognosis. Twelve patients, ranging in age from 24 to 59 years, with hypertension, proteinuria (greater than 1 g/d), and findings of benign nephrosclerosis on renal biopsy specimens were studied retrospectively. In three of these patients, the hypertension and proteinuria were diagnosed during pregnancy. Follow-up was possible in 11 patients. Nine patients became nephrotic in the course of their disease. Two patients had endstage renal disease and required maintenance dialysis treatment. Seven patients had decreased renal function as shown by the increase in serum creatinine levels. Thus, the combination of hypertension, proteinuria (greater than 1 g/d), and benign nephrosclerosis may be indicative of a progressive condition with a high percentage of patients having renal failure.