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R G McMorrow

Publications and source records attributed to R G McMorrow.

13 recordsLinked to original sources
PubMed1998

Epidemiology of IgA nephropathy in central and eastern Kentucky for the period 1975 through 1994. Central Kentucky Region of the Southeastern United States IgA Nephropathy DATABANK Project.

Population-based incidence data for IgA nephropathy (IgAN) are available for some countries but not for the United States. The purpose of this study was to determine the incidence of IgAN in central and eastern Kentucky for 5- and 10-yr periods between 1975 and 1994 and to examine differences among patient groups between those periods. The incidence of IgAN was 5.4 cases per one million population per year (MPPY) for period 1A (1975 through 1979), increasing to 12.4 cases per MPPY for period 2B (1990 through 1994) (P < 0.001). Males had a 2.7 times higher incidence than females for period 1 (1975 through 1984) and 2.2 times higher for period 2 (1985 through 1994). For period 1A, the incidence for Fayette County, which includes the city of Lexington, was lower than that of the rest of the study area (P=0.26), whereas for period 2 the incidence was higher for Fayette County (P=0.052). During period 1, the highest incidence of IgAN for any age and gender group was 24.3 cases per MPPY for males ages 30 through 39. For period 2, the incidence for males was similar for each decade between ages 20 and 59 (approximately 19 cases per MPPY). No African-American was diagnosed during period 1, but in period 2 incidences for blacks and whites were similar (10.7 and 10.2 cases per MPPY, respectively). For the last 5 yr of the study (1990 through 1994), the incidence of end-stage renal disease (ESRD) due to IgAN was 5.5 cases per MPPY: 8.4 for males and 2.7 for females. The incidence of IgAN in Kentucky for period 2B was still much lower than that in European studies, but the incidence of ESRD due to IgAN may be similar. Thus, IgAN may be as important a condition with respect to ESRD in Kentucky as it is in other regions of the world.

Adolescent↗
PubMed1988

Familial clustering and immunogenetic aspects of IgA nephropathy.

IgA nephropathy (IgAN) has been assumed to develop sporadically in individuals. We review the recent clinical and laboratory evidence that supports a genetic influence in the immunopathogenesis in some patients. These data include (1) families with multiple members with the disease not sharing a known nephrotoxic factor, (2) clustering of the birthplaces of ancestors of large pedigrees with multiple affected members, suggesting a "founder effect," (3) DNA alleles and protein phenotypes associated with IgAN (or a clinical subset) in some patient populations or that cosegregate with the disease in families with multiple affected members, and (4) immunologic abnormalities of patients shared by relatives with renal disease. However, the lack of understanding the fundamental pathogenetic mechanisms hinders progress in the pursuit of genetically controlled process in this disease. Furthermore, the diagnosis requires a renal biopsy, and no therapy has been proven effective. Therefore, asymptomatic family members with IgAN may forego the invasive diagnostic procedure necessary to establish the diagnosis, and instances of familial disease may not be investigated. Nonetheless, the increasing awareness of families with multiple affected members offers an opportunity to investigate the hypothesized genetic influence in the pathogenesis of IgAN.

Genetic Markers↗
PubMed1987

Morphologic and immunohistochemical observations in granulomatous glomerulonephritis.

Eight renal biopsies of Wegener's granulomatosis and other vasculitic syndromes with periglomerular granulomatous reactions (granulomatous glomerulonephritis) are studied. Controls consist of 57 biopsies of crescentic and focal necrotizing glomerulonephritis (of various diseases, excluding systemic lupus erythematosus). Both groups have in common the morphologic alterations of inflammatory tuft necrosis, fibrin exudation into the urinary space, crescent formation, and breaks of Bowman's capsule. In the study group, the unique feature of glomeruli with surrounding granulomatous reactions was the presence, within the urinary space, of an exudate of fibrin mixed with immune reactants (immunoglobulins and usually complement) in association with gaps of Bowman's capsule. This contrasts with an exudate of fibrin alone in glomeruli of the control group and other glomeruli of the study group. The study group also had a significantly greater incidence of immune deposits in Bowman's capsule (P less than 0.001). Giant cells may result from the interaction of macrophages of the granuloma with Bowman's capsule that is permeated with immune reactants.

Fluorescent Antibody Technique↗
PubMed1987

Regionalization in hereditary IgA nephropathy.

The genealogies of 80 patients with IgA nephropathy who were born in central or eastern Kentucky or whose parents were born in this region were researched. At a minimum, 48 of these patients were related to at least one other patient. On the basis of presence or absence of established kinships, the patients were divided into three groups. Twenty-nine patients in group 1 belonged to one large pedigree. Their birthplaces and those of their parents, grandparents, and great-grandparents clustered in the extreme eastern portion of the state. Seventeen other patients, group 2, were related to at least one other patient but not to a patient in group 1. Their birthplaces and those of their ancestors did not show significant clustering. With the exception of two siblings, the 34 patients of group 3 had no family members with IgA nephropathy. The birthplaces for these patients and ancestors were widely scattered. These data suggest that one or more genetically determined factors are important in the pathogenesis of IgA nephropathy in some patients. A founder effect, whereby a gene(s) conveying susceptibility to IgA nephropathy was carried into eastern Kentucky by one or more of the early settlers, would explain the geographic clustering of the birthplaces of the patients in group 1 and their ancestors. The characteristic immunopathology of IgA nephropathy may represent the histologic result of separate disease processes, one or more of which could be genetically influenced.

Consanguinity↗
PubMed1985

Focal sclerosis of hypertrophied glomeruli in solitary functioning kidneys of humans.

Morphometric data on glomerular size are presented on three patients with solitary functioning kidneys and one with bilateral oligomeganephronic hypoplasia. Renal biopsy of each of two patients with a congenitally absent kidney (unilateral renal agenesis) and a patient with oligomeganephronie, all with proteinuria and renal insufficiency, reveal increases of mean glomerular diameters of at least 1.75X and mean glomerular volumes greater than 5X. These dimensions, which are in the range of maximal increases recorded for man, are associated in all three biopsies with focal sclerosis of the hypertrophied glomeruli. By contrast, the functionally fully-compensated solitary kidney of a patient who lost function of the contralateral kidney from acquired disease, is characterized by the absence of focal glomerulosclerosis and by glomerular enlargement of significantly lesser degree (increased mean diameter 1.24X and mean volume less than 2X). These observations correlate glomerular injury with glomerular size and suggest that in the setting of reduced nephron numbers, nephron destruction via focal glomerulosclerosis may be initiated when compensatory glomerular hypertrophy has reached its limits.

Adult↗
PubMed1983

Serum complement proteins in IgA nephropathy.

Immunohistologic studies in IgA nephropathy which have suggested activation of the alternative complement pathway prompted us to study serum complement components and control proteins in 28 patients with IgA nephropathy. Thirteen patients, 12 of whom were men, had or developed chronic renal failure (CRF) during 34 +/- 5 months of follow-up. These patients were more hypertensive and had heavier proteinuria than those with stable renal function. Their serum IgA concentrations were not different from patients with normal renal function. The prevalence of HLA antigens was similar to that for the reference population and BW35 was not associated with CRF. Serum C3, B, H and I concentrations in patients with stable normal renal function were higher than they were in patients with CRF. Four patients studied--two with normal renal function and two with CRF--had partial familial deficiencies of single complement proteins. Our data suggest that high serum levels of C3, B, H and I may be associated with stable normal glomerular filtration rate and that complement deficiencies are not infrequent in IgA nephropathy. How these findings relate to the pathogenesis and progression of IgA nephropathy requires further study. We also conclude that higher serum IgA concentrations and the presence of BW35 are not necessarily associated with progressive renal insufficiency in IgA nephropathy.

Adult↗
PubMed1982

Quantitative urinary protein excretion in chronic renal failure.

The diagnostic value of the measurement of quantitative proteinuria in patients with a creatinine clearance of less than 10 ml/min was determined in patients seen in a single center over a 5-year period. All 126 patients in whom a definitive renal diagnosis was possible were included. Patients with glomerular disease excreted 6.1 +/- 0.6 g/day and patients with interstitial disease 1.5 +/- 0.3 g/day (p less than 0.001). In individual patients with end-stage renal disease, however, measurement of urinary protein excretion excluded (with 95% confidence levels) patients with interstitial diseases only when greater than 2.9 g/day. To examine the natural history of proteinuria in progressive renal disease, urinary protein, absolute and factored for glomerular filtration rate (GFR; creatinine clearance), was determined at 10 ml/min decrements in GFR for patients with membranoproliferative glomerulonephritis, idiopathic membranous glomerulonephritis and focal glomerulosclerosis. Quantitative urinary protein excretion was relatively constant as GFR fell but did fall significantly at less than 10 ml/min but only to 4.8-7.0 g/day at even that level. Urinary protein excretion/GFR increased as GFR fell, particularly at end stage where a highly significant four-fold rise was seen; an increase also occurred in patients with primary interstitial disease. Similar data were obtained for 34 randomly selected patients after at least 1 year of chronic hemodialysis. Although a significant decline in absolute urinary protein excretion occurred during the year of dialysis to levels not different between glomerular and interstitial disease, urinary protein excretion/unit GFR remained elevated. Increased urinary protein excretion/unit GFR may result from a functional adaptation of remaining nephrons in response to declining renal mass.

Creatinine↗
PubMed1980

Focal and segmental glomerular sclerosis in reflux nephropathy.

Reflux nephropathy was diagnosed in 23 patients (14 per cent of all the patients who received transplants) between 1973 and 1977, and nephrectomy was performed in all. Histology and immunofluorescence revealed a glomerular sclerosis associated with the idiopathic nephrotic syndrome. No focal and segmental glomerular sclerosis was seen in kidneys removed from patients with nonglomerular renal disease. Twenty-four hour urinary protein excretion in grams was 3.1 +/- 0.3 (mean +/- SEM) and was greater than that in our patients with end-stage nonglomerular renal disease. Thirty-one renal transplants were performed in these 23 patients; thereafter, maximum protein excretion was 1.4 g. Focal and segmental glomerular sclerosis was seen in only one (chronic rejection, protein excretion less than 0.5) of the 20 kidneys available for histologic study. Thus, focal and segmental glomerular sclerosis is extremely common in reflux nephropathy, accounts for "glomerular" proteinuria and may contribute importantly to progressive renal failure but, unlike that associated with the idiopathic nephrotic syndrome, rarely recurs after renal transplantation.

Adolescent↗
PubMed1980

Does vesicoureteric reflux result in renal allograft failure?

Vesicoureteric reflux (VUR) into transplanted kidneys has been cited as an often disregarded but frequent complication of transplantation which is associated with a glomerular lesion that resembles membranoproliferative glomerulonephritis, marked proteinuria, and graft failure. To determine the prevalence of this complication in our transplant population, all of our 23 patients with marked proteinuria and 27 controls without proteinuria had voiding cystourethrograms performed approximately two years after transplantation. In our population, VUR was infrequent (8%). Moreover, in the three of the four cases detected renal function has not deteriorated and three of the four do not have marked proteinuria. We cannot confirm the suggestion that VUR is a frequent cause of late renal allograft failure.

Adolescent↗
PubMed1980

Renal vein thrombosis in IgA nephropathy.

We report the first known case of renal vein thrombosis (RVT) in a patient with IgA nephropathy. We discuss the possible significance of this finding in support of the concept that RVT is a complication of glomerular disease.

Adult↗