Focal Segmental Glomerulosclerosis

Clinical Journal of the American Society of Nephrology, Journal Year: 2017, Volume and Issue: 12(3), P. 502 - 517

Published: Feb. 27, 2017

Focal segmental glomerulosclerosis (FSGS) is a leading cause of kidney disease worldwide. The presumed etiology primary FSGS plasma factor with responsiveness to immunosuppressive therapy and risk recurrence after transplant-important characteristics. In contrast, adaptive associated excessive nephron workload due increased body size, reduced capacity, or single glomerular hyperfiltration certain diseases. Additional etiologies are now recognized as drivers FSGS: high-penetrance genetic mutations in one nearly 40 genes, virus-associated FSGS, medication-associated FSGS. Emerging data support the identification sixth category: APOL1 allele-associated individuals sub-Saharan ancestry. classification particular patient relies on integration findings from clinical history, laboratory testing, biopsy, some patients, testing. biopsy can be helpful, clues provided by features light microscopy (

Language: Английский

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Transgenic expression of human APOL1 risk variants in podocytes induces kidney disease in mice

Nature Medicine, Journal Year: 2017, Volume and Issue: 23(4), P. 429 - 438

Published: Feb. 20, 2017

Language: Английский

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APOL1 Risk Variants Are Strongly Associated with HIV-Associated Nephropathy in Black South Africans

Journal of the American Society of Nephrology, Journal Year: 2015, Volume and Issue: 26(11), P. 2882 - 2890

Published: March 19, 2015

APOL1 variants are associated with HIV-associated nephropathy and FSGS in African Americans. The prevalence of these populations CKD HIV-1 infection has not been investigated. We determined the role 120 patients 108 controls from a South-African black population. Patients were selected on basis histology. Genotypes successfully for G1 G2 42 single nucleotide polymorphisms, including 18 ancestry informative markers, 116 (96.7%; 38 nephropathy, 39 HIV-positive CKD, HIV-negative CKD), (100%). Overall, 79% 2% population carried two risk alleles. In recessive model, individuals carrying any combination alleles had 89-fold higher odds (95% confidence interval, to 912; P<0.001) developing compared controls. Population allele frequencies 7.3% 11.1% G2. significantly other forms CKD. These results indicate HIV-positive, antiretroviral therapy-naïve blacks at very high nephropathy. Further studies required determine effect kidney diseases regions sub-Saharan Africa.

Language: Английский

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The next generation of therapeutics for chronic kidney disease

Nature Reviews Drug Discovery, Journal Year: 2016, Volume and Issue: 15(8), P. 568 - 588

Published: May 27, 2016

Language: Английский

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Acute Kidney Injury Due to Collapsing Glomerulopathy Following COVID-19 Infection

Kidney International Reports, Journal Year: 2020, Volume and Issue: 5(6), P. 940 - 945

Published: April 28, 2020

See Commentary on Page 759

Language: Английский

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Kidney disease in the setting of HIV infection: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference

Kidney International, Journal Year: 2018, Volume and Issue: 93(3), P. 545 - 559

Published: Feb. 3, 2018

HIV-positive individuals are at increased risk for kidney disease, including HIV-associated nephropathy, noncollapsing focal segmental glomerulosclerosis, immune-complex and comorbid as well injury resulting from prolonged exposure to antiretroviral therapy or opportunistic infections. Clinical guidelines disease prevention treatment in largely extrapolated studies the general population, do not fully incorporate existing knowledge of unique HIV-related pathways genetic factors that contribute this population. We convened an international panel experts nephrology, renal pathology, infectious diseases define pathology setting HIV infection; describe role genetics natural history, diagnosis, individuals; characterize risk-benefit prevention; best practices management individuals.

Language: Английский

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APOL1 kidney disease risk variants cause cytotoxicity by depleting cellular potassium and inducing stress-activated protein kinases

Proceedings of the National Academy of Sciences, Journal Year: 2015, Volume and Issue: 113(4), P. 830 - 837

Published: Dec. 23, 2015

Significance People of recent African ancestry develop chronic kidney disease and end stage failure at rates five times that European-Americans. Two coding variants in the apolipoprotein-L1 (APOL1) gene account for nearly all this excess risk. The mechanisms by which APOL1 cause are not understood. Recent evidence suggests transports cations, including K + , across lipid bilayers. Here, we show tetracycline-induced expression risk T-REx-293 cells causes significant net efflux intracellular which, turn, activates stress-activated protein kinases (SAPKs) p38 MAPK JNK, ultimately resulting cytotoxicity. We propose nephropathy may be mediated variant-induced loss aberrant activation SAPK signaling.

Language: Английский

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A tripartite complex of suPAR, APOL1 risk variants and αvβ3 integrin on podocytes mediates chronic kidney disease

Nature Medicine, Journal Year: 2017, Volume and Issue: 23(8), P. 945 - 953

Published: June 26, 2017

Language: Английский

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APOL1 Nephropathy: From Genetics to Clinical Applications

Clinical Journal of the American Society of Nephrology, Journal Year: 2020, Volume and Issue: 16(2), P. 294 - 303

Published: July 2, 2020

Rates of many types severe kidney disease are much higher in Black individuals than most other ethnic groups. Much this disparity can now be attributed to genetic variants the apoL1 (APOL1) gene found only with recent African ancestry. These greatly increase rates hypertension-associated ESKD, FSGS, HIV-associated nephropathy, and forms nondiabetic disease. We discuss population genetics APOL1 risk clinical spectrum nephropathy. then consider issues that arise for practicing nephrologist caring patient who may have

Language: Английский

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The glomerular filtration barrier: a structural target for novel kidney therapies

Nature Reviews Drug Discovery, Journal Year: 2021, Volume and Issue: 20(10), P. 770 - 788

Published: July 14, 2021

Language: Английский

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