scholarly journals A perspective on chronic kidney disease progression

2017 ◽  
Vol 312 (3) ◽  
pp. F375-F384 ◽  
Author(s):  
Jianyong Zhong ◽  
Hai-Chun Yang ◽  
Agnes B. Fogo

Chronic kidney disease (CKD) will progress to end stage without treatment, but the decline of renal function may not be linear. Compared with glomerular filtration rate and proteinuria, new surrogate markers, such as kidney injury molecule-1, neutrophil gelatinase-associated protein, apolipoprotein A-IV, and soluble urokinase receptor, may allow potential intervention and treatment in the earlier stages of CKD, which could be useful for clinical trials. New omic-based technologies reveal potential new genomic and epigenomic mechanisms that appear different from those causing the initial disease. Various clinical studies also suggest that acute kidney injury is a major risk for progressive CKD. To ameliorate the progression of CKD, the first step is optimizing renin-angiotensin-aldosterone system blockade. New drugs targeting endothelin, transforming growth factor-β, oxidative stress, and inflammatory- and cell-based regenerative therapy may have add-on benefit.

2018 ◽  
Vol 24 (9_suppl) ◽  
pp. 314S-322S
Author(s):  
Justin Lee ◽  
Ryan McMillan ◽  
Leonidas Skiadopoulos ◽  
Vinod Bansal ◽  
José Biller ◽  
...  

The prevalence of neurocognitive deficits remains high in patients with stage 5 chronic kidney disease (CKD5D). Major contributors to such deficits include stroke, cervical carotid artery disease (CCAD), and intracranial atherosclerotic disease (ICAD). The risk of developing these dysfunctional vascular processes is facilitated by the chronic inflammation associated with renal failure. Plasma levels of 10 circulating biomarkers in patients with CKD5D (n = 78-90) were quantified using the sandwich enzyme linked immune sorbent assay method. Biomarkers for this study included kidney injury molecule-1, N-terminal prohormone of brain natriuretic peptide (NT-proBNP), neutrophil gelatinase-associated lipocalin, interleukin-18, endothelin 1, calcifediol, parathyroid hormone, platelet-derived growth factor, microparticles-expressing tissue factor, and lipoprotein(a) (Lp(a)). Of the 90 patients with CKD5D, 30 had CCAD, 24 had ICAD, and 22 had stroke. Lp(a) level was significantly elevated in patients with CKD5D with comorbid ICAD compared to those without (125.70 ± 10.03 ng/mL vs 97.16 ± 5.97 ng/mL; P = .0065). NT-proBNP level was also significantly elevated in patients with CKD5D with comorbid stroke diagnosis compared to those without stroke history, once patients with a diagnosis of heart failure (HF) were excluded (14.84 ± 2.80 ng/mL vs 9.06 ± 1.27 ng/mL; P = .0283). Profiling levels of Lp(a) and NT-ProBNP could thus be useful in the risk stratification of ICAD and stroke, respectively, in the CKD5D population.


2021 ◽  
pp. 189-190
Author(s):  
G.G. Kaushik ◽  
Shubham Maheshwari ◽  
Ankita Sharma

Introduction: Serum lipocalin 2 serve as a marker for kidney function. Lipocalin 2 is found in both CKD and kidney injury and it rises in acute kidney injury (AKI) and in patients have faster decline in kidney function. Aims And Objectives: To nd out correlation and assess of serum Neutrophil gelatinase-associated lipocalin 2 (NGAL 2) in patients with stages 2 to 4 of Chronic Kidney disease. The aim of the study was NGAL could represent a novel, sensitive marker of kidney function in adult patients with CKD. Material And Methods: Study involved 120 patients divided in Case group (60 patients) attended medical/ urology OPD or admitted in medical/urology ward of CKD2 – CKD4 while control group – age and sex matched healthy individuals/ stage I CKD patients was taken as control. The plasma/ serum were used for serum urea, creatinine, Cystatin C and lipocalin 2 under all aseptic precaution on receiving consent. Result:The patients of CKD included in study were having glomerulonephritis (46.7%), pyelonephritis (21.7%), diabetic kidney disease (13.3%), polycystic kidney disease (1.7%) and other causes (16.7%). CKD patients demonstrated elevated serum NGAL 159.14 ± 48.73 ng/ml, together with a rise in urea 59.9 ± 17.6 mg/dL, serum creatinine 1.56 ± 0.97 mg/dL and Cystatin C 199 ± 113 ng/ml as compared to control have serum NGAL 76.31 ± 26.34 ng/ml, urea 22.3 ± 5.7 mg/dL, serum creatinine 0.75 ± 0.14 mg/dL and Cystatin C 76 ± 17 ng/ml (P value <0.05). Conclusion: Serum NGAL closely correlates with serum Cystatin C, creatinine, and eGFR, and serve as a potential early and sensitive marker of impaired kidney function/ kidney injury.


Author(s):  
Natalie Ebert ◽  
Elke Schaeffner

Both acute and chronic states of kidney disease have considerable healthcare impact as they can produce enormous disease burden and costs. To classify chronic kidney disease into the CKD staging system, glomerular filtration rate as an index of kidney function, as well as albuminuria as a marker of kidney damage have to be assessed as correctly as possible. Misclassification is a serious concern due to the difficulties in precise GFR assessment and correct interpretation of results. Differentiating between pure senescence and true disease among older adults can be a delicate issue. To find the right renal replacement option for individuals that progress to end-stage renal disease can be challenging, and some older patients may even benefit from conservative care without dialysis. To prevent acute kidney injury as a frequent and potentially life-threatening complication, clinicians need to develop an understanding of the common vulnerability to kidney damage among older adults.


Author(s):  
SHAREEF J. ◽  
SRIDHAR S. B. ◽  
SHARIFF A.

Proton pump inhibitors (PPIs) are most widely used medications for acid related gastrointestinal disorders. Accessible evidence based studies suggest that the increased use of PPI is linked to a greater risk of developing kidney diseases. This review aims to determine the association of kidney disease with the use of proton pump inhibitor with various study designs. PubMed, Scopus and Google Scholar databases as well as a reference list of relevant articles were systematically searched for studies by using the following search terms; ‘proton pump inhibitors’, ‘acute kidney injury’, ‘chronic kidney disease’ and ‘end stage renal disease’. Both observational and randomized controlled trials (RCTs) exploring the association of PPI use with kidney disease were eligible for inclusion. A total of 8 articles, including 9 studies (n = 794,349 participants) were identified and included in the review. Majority of the studies showed a higher risk of kidney outcomes in patients taking PPIs, with effect higher of acute kidney injury (4-to 6-fold) compared with chronic kidney disease and end stage renal disease (1.5-to 2.5-fold). However, the studies suggest that the strength of evidence is weak and could not prove causation. The risk increased considerably with the use of high dose of PPIs and prolonged duration of exposure necessitates the monitoring of renal function. Exercising vigilance in PPI use and cessation of proton pump inhibitor when there is no clear indication may be a reasonable approach to reduce the population burden of kidney diseases.


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