Management of chronic renal insufficiency in lupus nephritis: Role of                 proteinuria, hypertension and dyslipidemia in the progression of renal disease

Background: We conducted single-marker, gene-based and pathway-based analyses to examine the association between renin-angiotensin-aldosterone system (RAAS) variants and chronic kidney disease (CKD) progression among Chronic Renal Insufficiency Cohort (CRIC) study participants. Methods: A total of 1,523 white and 1,490 black subjects were genotyped for 490 SNPs in 12 RAAS genes as part of the ITMAT-Broad-CARe array. CKD progression phenotypes included decline in estimated glomerular filtration rate (eGFR) over time and the occurrence of a renal disease event, defined as incident end stage renal disease or halving of eGFR from baseline. Mixed-effects models were used to examine SNP associations with eGFR decline, while Cox proportional hazards models tested SNP associations with renal events. Gene and pathway-based analyses were conducted using the truncated product method. All analyses were stratified by race, and a Bonferroni correction was applied to adjust for multiple testing. Results: Among white and black participants, eGFR declined an average of 1.2 and 2.3 ml/min/1.73m 2 per year, respectively, while renal events occurred in a respective 11.5% and 24.9% of participants. We identified strong gene and pathway-based associations with CKD progression. The AGT and RENBP genes were consistently associated with risk of renal events in separate analyses of white and black participants (all P <1.00х10 -6 ). Driven by the significant gene-based findings, the entire RAAS pathway was also associated with renal events in both groups (both P <1.00х10 -6 ). No single-marker associations with CKD progression were observed. Conclusions: The current study provides strong evidence for a role of the RAAS in CKD progression.

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The role of decreased levels of antimicrobian peptides in progression of chronic renal insufficiency

International Journal of Contemporary Research and Review ◽

10.15520/ijcrr/2016/7/12/23 ◽

2016 ◽

Vol 7 (12) ◽

Author(s):

Goyushova R.R. ◽

Aliyev A. H. ◽

Ibrahimova S. Sh ◽

Mammadova N. T.

Keyword(s):

Renal Insufficiency ◽

Chronic Renal Insufficiency

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Chronic renal insufficiency among Asian Indians with type 2 diabetes: I. Role of RAAS gene polymorphisms

BMC Medical Genetics ◽

10.1186/1471-2350-7-42 ◽

2006 ◽

Vol 7 (1) ◽

Cited By ~ 41

Author(s):

Pushplata Prasad ◽

Arun K Tiwari ◽

KM Prasanna Kumar ◽

AC Ammini ◽

Arvind Gupta ◽

...

Keyword(s):

Type 2 Diabetes ◽

Renal Insufficiency ◽

Chronic Renal Insufficiency ◽

Gene Polymorphisms ◽

Asian Indians

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Glomerular Hematuria: Cause or Consequence of Renal Inflammation?

International Journal of Molecular Sciences ◽

10.3390/ijms20092205 ◽

2019 ◽

Vol 20 (9) ◽

pp. 2205 ◽

Cited By ~ 8

Author(s):

Juan Antonio Moreno ◽

Ángel Sevillano ◽

Eduardo Gutiérrez ◽

Melania Guerrero-Hue ◽

Cristina Vázquez-Carballo ◽

...

Keyword(s):

Renal Disease ◽

Red Blood Cells ◽

Blood Cells ◽

Cell Injury ◽

Kidney Injury ◽

Inflammatory Cytokine Production ◽

Progression Of Renal Disease ◽

Cardinal Symptom ◽

Urinary Space

Glomerular hematuria is a cardinal symptom of renal disease. Glomerular hematuria may be classified as microhematuria or macrohematuria according to the number of red blood cells in urine. Recent evidence suggests a pathological role of persistent glomerular microhematuria in the progression of renal disease. Moreover, gross hematuria, or macrohematuria, promotes acute kidney injury (AKI), with subsequent impairment of renal function in a high proportion of patients. In this pathological context, hemoglobin, heme, or iron released from red blood cells in the urinary space may cause direct tubular cell injury, oxidative stress, pro-inflammatory cytokine production, and further monocyte/macrophage recruitment. The aim of this manuscript is to review the role of glomerular hematuria in kidney injury, the role of inflammation as cause and consequence of glomerular hematuria, and to discuss novel therapies to combat hematuria.

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