scholarly journals Rethinking glomerular basement membrane thickening in diabetic nephropathy: adaptive or pathogenic?

2016 ◽  
Vol 311 (5) ◽  
pp. F831-F843 ◽  
Author(s):  
Caroline B. Marshall
Keyword(s):  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Biological Significance ◽  
Clinical Manifestations ◽  
Silent Period ◽  
The United States ◽  
End Stage ◽  
Gbm Thickening

Diabetic nephropathy (DN) is the leading cause of chronic kidney disease in the United States and is a major cause of cardiovascular disease and death. DN develops insidiously over a span of years before clinical manifestations, including microalbuminuria and declining glomerular filtration rate (GFR), are evident. During the clinically silent period, structural lesions develop, including glomerular basement membrane (GBM) thickening, mesangial expansion, and glomerulosclerosis. Once microalbuminuria is clinically apparent, structural lesions are often considerably advanced, and GFR decline may then proceed rapidly toward end-stage kidney disease. Given the current lack of sensitive biomarkers for detecting early DN, a shift in focus toward examining the cellular and molecular basis for the earliest structural change in DN, i.e., GBM thickening, may be warranted. Observed within one to two years following the onset of diabetes, GBM thickening precedes clinically evident albuminuria. In the mature glomerulus, the podocyte is likely key in modifying the GBM, synthesizing and assembling matrix components, both in physiological and pathological states. Podocytes also secrete matrix metalloproteinases, crucial mediators in extracellular matrix turnover. Studies have shown that the critical podocyte-GBM interface is disrupted in the diabetic milieu. Just as healthy podocytes are essential for maintaining the normal GBM structure and function, injured podocytes likely have a fundamental role in upsetting the balance between the GBM's synthetic and degradative pathways. This article will explore the biological significance of GBM thickening in DN by reviewing what is known about the GBM's formation, its maintenance during health, and its disruption in DN.

scholarly journals A Case of Anti-Glomerular Basement Membrane Crescentic Glomerulonephritis in a Female Renal Allograft Recipient with Unknown Native Disease: Retrospective Molecular Confirmation of Alport Disease

2019 ◽  
Vol 12 (1) ◽  
pp. 35-40
Author(s):  
Mahesha Vankalakunti ◽  
Ashish Parekh ◽  
Anil K. B. Thimmegowda ◽  
Rajanna Sreedhara
Keyword(s):  
Kidney Disease ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Renal Allograft ◽  
Crescentic Glomerulonephritis ◽  
Deceased Donor ◽  
Renal Allograft Recipient ◽  
End Stage Kidney Disease ◽  
Allograft Outcome ◽  
End Stage

Anti-Glomerular Basement Membrane (anti-GBM) crescentic glomerulonephritis developing in an allograft is a rare phenomenon. A patient with Alport syndrome receiving a renal transplant is at risk of developing anti-GBM glomerulonephritis, due to the absence of normal COL4α3, COL4α4 and COL4α5 trimer of the collagen network. Two unique challenges with planning kidney transplant in such a patient include- ideal donor selection; and risk of developing anti-GBM nephritis. We report a case of post-transplant anti-GBM crescentic glomerulonephritis in a female recipient with unknown native kidney disease who was diagnosed with Alport disease when she presented with hematuria and proteinuria nearly 2 years postrenal transplant. Allograft outcome in our case was unfavourable, patient reaching end-stage kidney disease within 6-month of diagnosis. The patient remains on continuous ambulatory peritoneal dialysis and currently active on the deceased donor transplant waiting list.

scholarly journals End-Stage Kidney Disease From Scleroderma in the United States, 1996 to 2012

2018 ◽  
Vol 3 (1) ◽  
pp. 148-154 ◽  
Author(s):  
Donal J. Sexton ◽  
Scott Reule ◽  
Robert N. Foley
Keyword(s):  
United States ◽  
Kidney Disease ◽  
The United States ◽  
End Stage Kidney Disease ◽  
End Stage

scholarly journals Outcomes Associated With Apixaban Use in Patients With End-Stage Kidney Disease and Atrial Fibrillation in the United States

Circulation ◽  
2018 ◽  
Vol 138 (15) ◽  
pp. 1519-1529 ◽  
Author(s):  
Konstantinos C. Siontis ◽  
Xiaosong Zhang ◽  
Ashley Eckard ◽  
Nicole Bhave ◽  
Douglas E. Schaubel ◽  
...  
Keyword(s):  
United States ◽  
Atrial Fibrillation ◽  
Kidney Disease ◽  
The United States ◽  
End Stage Kidney Disease ◽  
End Stage

Diabetic kidney disease in thedb/dbmouse

2003 ◽  
Vol 284 (6) ◽  
pp. F1138-F1144 ◽  
Author(s):  
Kumar Sharma ◽  
Peter McCue ◽  
Stephen R. Dunn
Keyword(s):  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Mouse Model ◽  
Renal Disease ◽  
Mouse Models ◽  
Diabetic Kidney Disease ◽  
Diabetic Kidney ◽  
Matrix Expansion ◽  
Stage Renal Disease ◽  
End Stage

Diabetic nephropathy is increasing in incidence and is now the number one cause of end-stage renal disease in the industrialized world. To gain insight into the genetic susceptibility and pathophysiology of diabetic nephropathy, an appropriate mouse model of diabetic nephropathy would be critical. A large number of mouse models of diabetes have been identified and their kidney disease characterized to various degrees. Perhaps the best characterized and most intensively investigated model is the db/ db mouse. Because this model appears to exhibit the most consistent and robust increase in albuminuria and mesangial matrix expansion, it has been used as a model of progressive diabetic renal disease. In this review, we present the findings from various studies on the renal pathology of the db/ db mouse model of diabetes in the context of human diabetic nephropathy. Furthermore, we discuss shortfalls of assessing functional renal disease in mouse models of diabetic kidney disease.

Chronic Kidney Failure and Dialysis

2018 ◽  
Author(s):  
Raghu V Durvasula ◽  
Jonathan Himmelfarb
Keyword(s):  
United States ◽  
Chronic Kidney Disease ◽  
Peritoneal Dialysis ◽  
Kidney Disease ◽  
Renal Disease ◽  
Chronic Renal Disease ◽  
Clinical Manifestations ◽  
Kidney Injury ◽  
The United States ◽  
Clinical Syndrome

Chronic kidney disease (CKD) is a clinical syndrome arising from progressive kidney injury, formerly known as chronic renal failure, chronic renal disease, and chronic renal insufficiency. It is classified into five stages based primarily on glomerular filtration rate (GFR). This article discusses the epidemiology of CKD and end-stage renal disease (ESRD), as well as etiology and genetics, pathophysiology, and pathogenesis. The section on diagnosis looks at clinical manifestations and physical findings, laboratory (and other) tests, imaging studies, and biopsy. A short section on differential diagnosis is followed by a discussion of treatment, including hemodialysis and peritoneal dialysis. Long-term complications of patients on dialysis include cardiovascular disease, renal osteodystrophy, dialysis-related amyloidosis, and acquired cystic disease (renal cell carcinoma). The final section addresses prognosis and socioeconomic burden. Figures include the classification system for CKD, prevalence of CKD in the United States, rising prevalence, risk of, and leading causes of ESRD in the United States, plus the changing prevalence of ESRD over time, clinical manifestations of uremia, and an overview of hemodialysis circuit. Tables look at the burden of CKD relative to other chronic disorders, the specific hereditary causes of kidney disease, and situations when serum creatinine does not accurately predict GFR. Other tables list equations for estimating GFR, the causes of CKD without shrunken kidneys, and clinical features distinguishing chronic kidney disease from acute kidney injury. ESRD and indications for initiation of dialysis are presented, as well as typical composition of dialysate and reasons for failure of peritoneal dialysis. This chapter contains 71 references.

Sign in / Sign up

Export Citation Format

Share Document