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Table of Contents
Year : 2018  |  Volume : 4  |  Issue : 3  |  Page : 59-60

Progressive Nature of Chronic Kidney Disease

Sr. Consultant and HOD, Department of Nephrology, Venkateshwar Hospital, New Delhi, India

Date of Web Publication23-Apr-2019

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrnm.jrnm_15_19

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How to cite this article:
Varma PP. Progressive Nature of Chronic Kidney Disease. J Renal Nutr Metab 2018;4:59-60

How to cite this URL:
Varma PP. Progressive Nature of Chronic Kidney Disease. J Renal Nutr Metab [serial online] 2018 [cited 2020 Feb 21];4:59-60. Available from: http://www.jrnm.in/text.asp?2018/4/3/59/256817

  Introduction Top

Chronic kidney disease (CKD) is defined as an irreversible and progressive deterioration of kidney function of at least 3-month duration. With increasing prevalence of diabetes, hypertension, and increasing life span, the prevalence of CKD is increasing globally. In India, 10%–13% of the population has CKD. A minority of CKD patients progresses to end-stage kidney failure, but CKD is a strong risk factor for cardiovascular morbidity and mortality; therefore, it is important to recognize CKD early and to put preventive strategies in place.[1],[2]

Recent data show that in a large number of patients, ~40% CKD Stage III may not be progress/slowly progress (glomerular filtration rate loss <1 ml/min/year), while in others, progression may be faster (renal function loss >3 ml/min/year). Importantly, progression of kidney disease in the majority (~75%) is nonlinear. Those CKD patients with proteinuria, hypertension, and advanced stage of CKD have faster progression while elderly CKD patients progress slower. Proteinuria remains the most important risk factor of progression whether CKD patient is a diabetic or nondiabetic.

  Pathophysiology Top

Some of the important risk factors for progression of CKD are (i) race and genetics, (ii) glomerular hypertension, (iii) proteinuria, (iv) high protein diet, (v) dyslipidemia, (vi) hyperuricemia, and (vii) acidosis.[3] American-Africans have faster progression of CKD. Race and genetics do play an important role in the progression of CKD although this is not a modifiable factor. renin–angiotensin–aldosterone system (RAAS) plays an important role as many profibrotic actions of the RAAS are mediated directly by AngII. AngII promotes migration of endothelial and vascular smooth muscle cells and hypertrophy and hyperplasia of smooth muscle cells and mesangial cells. All components of the RAS are present in macrophages, which may thus serve as yet another source of AngII and also respond to angiotensin-converting enzyme inhibitor (ACEI) and angiotensin receptor blocker (ARB). Besides that, many cytokines play a role in the progression of CKD. AngII also induces other growth factors, including basic fibroblast growth factor, platelet-derived growth factor, transforming growth factor-β, and plasminogen activator inhibitor-1 (PAI-1), all of which may impact on fibrosis. New data indicate that aldosterone has both genomic and nongenomic actions to promote fibrosis, independent of its actions to increase blood pressure (BP) by mediating salt retention. Aldosterone enhances angiotensin induction of PAI-1 and also has direct actions on fibrosis. Conversely, aldosterone receptor antagonism with spironolactone decreases injury.

  Strategies to Slow the Progression Top

ACEIs/ARBs help reduce intraglomerular hypertension and proteinuria, irrespective of the hypertension state. By blocking AngII, they check fibrosis and slow the progression. They remain the most important instrument of prevention. Likewise good BP control <140/90 mm Hg and <130/80 mm Hg in proteinuric patients, good glycemic control (hemoglobin A1c <7) and good lipid control are important strategies to slow the progression. Recent data suggest that ketoanalogs (KAs) and uric acid control too probably help in slowing the progression.[4],[5]

  Conclusions Top

All CKD patients do not progress equally fast. There is need to identify those who are progress faster. These patients should get due care with ACE/ARBs and good control of BP, diabetes, and lipids. Diet, KA, and uric acid control are emerging strategies.

  References Top

Drawz PE, Rosenberg ME. Slowing progression of chronic kidney disease. Kidney Int Suppl (2011) 2013;3:372-6.  Back to cited text no. 1
Varma PP. Prevalence of chronic kidney disease in India – Where are we heading? Indian J Nephrol 2015;25:133-5.  Back to cited text no. 2
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Kovesdy CP. Metabolic acidosis and kidney disease: Does bicarbonate therapy slow the progression of CKD? Nephrol Dial Transplant 2012;27:3056-62.  Back to cited text no. 3
Wu CH, Yang YW, Hung SC, Kuo KL, Wu KD, Wu VC, et al. Ketoanalogues supplementation decreases dialysis and mortality risk in patients with anemic advanced chronic kidney disease. PLoS One 2017;12:e0176847.  Back to cited text no. 4
Nacak H, van Diepen M, Qureshi AR, Carrero JJ, Stijnen T, Dekker FW, et al. Uric acid is not associated with decline in renal function or time to renal replacement therapy initiation in a referred cohort of patients with Stage III, IV and V chronic kidney disease. Nephrol Dial Transplant 2015;12:2039-45  Back to cited text no. 5


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