Focal and segmental glomerular sclerosis in reflux nephropathy

Bhathena, Dinyar; Weiss, Jay H.; Holland, Nancy H.; McMorrow, Rita; Curtis, John J.; Lucas, Bruce A.; Luke, Robert G.

doi:10.1016/0002-9343(80)90218-1

Cited by 100 publications

(26 citation statements)

References 23 publications

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“…The pathogenesis is unknown, but substantial evidence suggests that direct viral or toxic GEC injury or circulating permeability factor(s) lead to GEC damage and consequent formation of the characteristic segmental lesions. The factors which distinguish primary and secondary FSGS consist of: (1) absence of a disease which can cause FSGS, including, specifically, hypertension and reduced nephron mass at presentation; (2) the presence of GEC damage ultrastructurally prior to change in renal function; (3) the presence of a variety of circulating permeability factors which can induce proteinuria in experimental animals and cause immediate proteinuria in the transplanted graft, suggesting a soluble factor as a pathogenetic process, and (4) a high rate of recurrence in a transplanted kidney as opposed to other forms of FSGS [8, 9]. Morphologically, primary FSGS can be categorized into three forms [5, 10, 11]: (1) classic FSGS with segmental areas of hyalinosis and segmental glomerular collapse near the vascular pole associated with adhesions between the collapsed area and Bowman’s capsule; (2) ‘tip’ lesions with segmental collapse of capillary loops and GEC proliferation at the tubular pole of the glomerulus, and (3) ‘collapsing’ glomerulopathy associated with GEC proliferation, expansion of Bowman’s space, loss of classic podocyte phenotype and transdifferentiation of podocytes into macrophage-like cells [12, 13].…”

Section: Primary Fsgsmentioning

confidence: 99%

Pathogenesis of Focal Glomerulosclerosis

Bolton¹,

Abdel‐Rahman²

2001

Nephron

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Focal segmental glomerulosclerosis (FSGS) is the histologic expression of diverse processes affecting the renal glomeruli and occurring in primary and secondary forms. A number of pathogenic factors have been identified in primary FSGS, and multiple etiologies have been defined as contributing factors for the development of secondary FSGS. There is a complex interplay between etiologic and pathogenic factors, progression factors and intervention in the phenotypic expression of FSGS. Key components include genetic predisposition, environmental influences and the impact on phenotype of pharmacologic intervention. The phenotypic spectrum for FSGS ranges from mild proteinuria and slow progression to a devastating clinical syndrome characterized by heavy proteinuria and rapid loss of renal function over a period of months. While the pathogenesis is unknown, much is known about factors which are involved in the development and progression of both primary and secondary FSGS. The ultimate goal of understanding pathogenesis is to provide specific nontoxic therapy for those patients who have a definable form of FSGS. While this goal is not yet in sight, many types of intervention, not addressed in the current chapter, can influence the course of various diseases presenting as FSGS. Until specific therapy can be fashioned, it is necessary for the clinician caring for these patients to appreciate the complex interaction of pathogenetic factors involved in the development and pregression of FSGS, as a rationale for providing intervention to prevent development of the disease and to slow its course.

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Section: Primary Fsgsmentioning

confidence: 99%

Pathogenesis of Focal Glomerulosclerosis

Bolton¹,

Abdel‐Rahman²

2001

Nephron

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“…As a result of our investigations, we are able to con clude that glomerular lesions comparable to those found in subtotally nephrectomized rats are not only found in patients with reflux nephropathy [15,[24][25][26].…”

Section: Discussionmentioning

confidence: 85%

Hyperperfusion Injury of the Human Kidney in Different Glomerular Diseases

1988

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Investigations of biopsy material from human kidneys with different forms of glomerulonephritis (n = 1,240) and with diabetic glomerulosclerosis (n = 406) performed in order to find changes caused by hyperperfusion of the kidney tissue gave the following results: (1) Hyperperfusion injury occurs in the different forms of glomerulonephritis with varying frequency. It was rarely found in immunologically negative mesangioproliferative glomerulonephritis. The highest incidence was found in patients with membranoproliferative glomerulonephritis type I. (2) Hyperperfusion injury was also found in kidneys with diabetic glomerulosclerosis. The frequency of this finding increased with the degree of the diabetic changes. (3) The hyperperfusion injury was seen as a complication of glomerulonephritis or diabetic glomerulosclerosis only when the patient clinically had developed malignant hypertension and when the serum creatinine level was elevated, a sign of compensated retention. (4) In patients with glomerulonephritis, the hyperperfusion changes occurred more frequently in males than in females. Diabetic glomerulosclerosis was complicated by hyperperfusion injury with the same frequency in both sexes. (5) Patients with hyperperfusion changes of the kidneys always excrete large amounts of protein in the urine. (6) Hyperperfusion changes occur first in the juxtamedullary glomeruli. The intermediate glomeruli are affected later and the subcapsular glomeruli last.

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“…Alternatively, reflux nephropathy and hereditary nephritis may have glomerular lesions responsible for high levels of urine protein. In support of this alternative are the studies of Bhalhena et al [14] demonstrating focal segmental glomerular sclerosis in patients with reflux nephropathy and of O'Neill et al [15] suggesting that hereditary nephritis has an important glo merular component.…”

Section: Discussionmentioning

confidence: 94%

Quantitative Urinary Protein Excretion in Chronic Renal Failure

McMorrow¹,

Galla²,

Luke³

1982

Am J Nephrol

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The diagnostic value of the measurement of quantitative proteinuria in patients with a creatinine clearance of < 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 < 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 > 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 < 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.

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Focal and segmental glomerular sclerosis in reflux nephropathy

Cited by 100 publications

References 23 publications

Pathogenesis of Focal Glomerulosclerosis

Pathogenesis of Focal Glomerulosclerosis

Hyperperfusion Injury of the Human Kidney in Different Glomerular Diseases

Quantitative Urinary Protein Excretion in Chronic Renal Failure

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