The relationship between urinary kidney injury molecule-1 and blood bone metabolism markers in patients with chronic kidney disease

2020 ◽  
Vol 93 (2) ◽  
pp. 65-76 ◽  
Author(s):  
Caixia Yin ◽  
Chen Cheng ◽  
Jing Wang ◽  
Lina Zhang ◽  
Yogendranath Purrunsing ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Metabolism ◽  
Kidney Injury ◽  
Bone Metabolism Markers ◽  
Kidney Injury Molecule 1 ◽  
The Relationship

scholarly journals Circulating Biomarker Levels in Patients With Stage 5 Chronic Kidney Disease With Respect to Neurovascular Diseases

2018 ◽  
Vol 24 (9_suppl) ◽  
pp. 314S-322S
Author(s):  
Justin Lee ◽  
Ryan McMillan ◽  
Leonidas Skiadopoulos ◽  
Vinod Bansal ◽  
José Biller ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Carotid Artery Disease ◽  
Kidney Injury ◽  
Assay Method ◽  
Neurocognitive Deficits ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Intracranial Atherosclerotic Disease ◽  
Artery Disease ◽  
Kidney Injury Molecule 1

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.

scholarly journals PGC1α in the kidney

2018 ◽  
Vol 314 (1) ◽  
pp. F1-F8 ◽  
Author(s):  
Matthew R. Lynch ◽  
Mei T. Tran ◽  
Samir M. Parikh
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Renal Fibrosis ◽  
Diabetic Kidney Disease ◽  
Kidney Injury ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
The Relationship ◽  
Prime Target

Acute kidney injury (AKI) arising from diverse etiologies is characterized by mitochondrial dysfunction. The peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC1α), a master regulator of mitochondrial biogenesis, has been shown to be protective in AKI. Interestingly, reduction of PGC1α has also been implicated in the development of diabetic kidney disease and renal fibrosis. The beneficial renal effects of PGC1α make it a prime target for therapeutics aimed at ameliorating AKI, forms of chronic kidney disease (CKD), and their intersection. This review summarizes the current literature on the relationship between renal health and PGC1α and proposes areas of future interest.

scholarly journals Beyond the tubule: pathological variants of LRP2, encoding the megalin receptor, result in glomerular loss and early progressive chronic kidney disease

2020 ◽  
Vol 319 (6) ◽  
pp. F988-F999
Author(s):  
Jennifer R. Charlton ◽  
Weizhen Tan ◽  
Ghaleb Daouk ◽  
Lisa Teot ◽  
Seymour Rosen ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Kidney Injury ◽  
Glomerular Proteinuria ◽  
Increased Risk ◽  
Kidney Injury Molecule 1 ◽  
Deficient Mice

Pathogenic variants in the LRP2 gene, encoding the multiligand receptor megalin, cause a rare autosomal recessive syndrome: Donnai-Barrow/Facio-Oculo-Acoustico-Renal (DB/FOAR) syndrome. Because of the rarity of the syndrome, the long-term consequences of the tubulopathy on human renal health have been difficult to ascertain, and the human clinical condition has hitherto been characterized as a benign tubular condition with asymptomatic low-molecular-weight proteinuria. We investigated renal function and morphology in a murine model of DB/FOAR syndrome and in patients with DB/FOAR. We analyzed glomerular filtration rate in mice by FITC-inulin clearance and clinically characterized six families, including nine patients with DB/FOAR and nine family members. Urine samples from patients were analyzed by Western blot analysis and biopsy materials were analyzed by histology. In the mouse model, we used histological methods to assess nephrogenesis and postnatal renal structure and contrast-enhanced magnetic resonance imaging to assess glomerular number. In megalin-deficient mice, we found a lower glomerular filtration rate and an increase in the abundance of injury markers, such as kidney injury molecule-1 and N-acetyl-β-d-glucosaminidase. Renal injury was validated in patients, who presented with increased urinary kidney injury molecule-1, classical markers of chronic kidney disease, and glomerular proteinuria early in life. Megalin-deficient mice had normal nephrogenesis, but they had 19% fewer nephrons in early adulthood and an increased fraction of nephrons with disconnected glomerulotubular junction. In conclusion, megalin dysfunction, as present in DB/FOAR syndrome, confers an increased risk of progression into chronic kidney disease.

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
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Transforming Growth Factor ◽  
Kidney Injury ◽  
Transforming Growth Factor Β ◽  
New Drugs ◽  
Kidney Disease Progression ◽  
Kidney Injury Molecule 1 ◽  
End Stage ◽  
Neutrophil Gelatinase

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.

Chronic Kidney Disease: Detection and Evaluation

2020 ◽  
pp. 12-19
Author(s):  
Raena Pettitt ◽  
Alonna Brumbaugh ◽  
Michaela Gartman ◽  
Alyssa Jackson
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Accurate Determination ◽  
Kidney Injury ◽  
Screening Tests ◽  
Kidney Size ◽  
Early Stages ◽  
Urine Albumin ◽  
Asymptomatic Patients ◽  
Kidney Injury Molecule 1

Chronic kidney disease (CKD) is a prevalent disease that continues to affect more than one-tenth of the American population. Early detection is essential to slow the natural progression of CKD. This can be accomplished by urine and blood screening tests, which are analyzed for creatinine, urine albumin, and urine protein. Screening is often indicated for individuals with known comorbidities such as cardiovascular disease, mineral and bone disorders, and diabetes. Asymptomatic patients with early renal disease can make detection problematic, requiring clinicians to recognize risk factors that may warrant further testing. When symptoms do appear, the renal manifestations are often broad, including changes in kidney size, electrolyte abnormalities, and proteinuria. Changes in biomarkers may be evaluated in the early stages of CKD before significant kidney damage. The current, most accurate determination of renal function is the estimated glomerular filtration rate (GFR), which must be less than 60 mL/min to prompt further testing for CKD. Novel biomarkers may allow for earlier diagnosis of CKD as they can be detected at lower levels than standard biomarkers. Biomarkers such as homocysteine, cystatin C, and kidney injury molecule-1 are predicted to become more prevalent in a clinical setting. The current gold standard for diagnosis of CKD is a renal biopsy, but MRI is a less invasive alternative. Proper staging of CKD allows for appropriate evaluation and treatment of the patient. The early stages of CKD should be treated to limit complications and to prolong the life and health of patients.

N-acteyl-ß-D-glucosaminidase and kidney injury molecule-1: New predictors for long-term progression of chronic kidney disease in patients with heart failure

Nephrology ◽  
2016 ◽  
Vol 21 (6) ◽  
pp. 490-498 ◽  
Author(s):  
Carsten G. Jungbauer ◽  
Ekrem Uecer ◽  
Stefan Stadler ◽  
Christoph Birner ◽  
Stefan Buchner ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Patients With Heart Failure ◽  
Kidney Injury Molecule 1

scholarly journals Evaluation of the Urinary Kidney Injury Molecule-1 Levels in Patients With Diabetic Nephropathy

2014 ◽  
Vol 37 (6) ◽  
pp. 377 ◽  
Author(s):  
Buket Kin Tekce ◽  
Hikmet Tekce ◽  
Gulali Aktas ◽  
Mustafa Sit
Keyword(s):  
Chronic Kidney Disease ◽  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Urinary Albumin Excretion ◽  
Kidney Injury ◽  
Urinary Albumin ◽  
Disease Stage ◽  
Tubular Damage ◽  
Albumin Excretion ◽  
Kidney Injury Molecule 1

Purpose: Kidney Injury Molecule-1 is a protein that increases in urine following tubular damage. Kidney Injury Molecule-1 levels were correlated with the level of chronic kidney disease secondary to diabetic nephropathy in patients with type 2 Diabetes Mellitus. Methods: Clinical and laboratory findings of 142 patients with diabetic nephropathy and 34 control subjects were analysed. Creatinine and HbA1c levels in blood samples and albumin, creatinine and Kidney Injury Molecule-1 levels in urine samples were assessed. Results: Urinary Kidney Injury Molecule-1 levels were significantly increased both in subgroups of diabetic nephropathy (normo-/micro-/macro-albuminuria) and in chronic kidney disease (stage 2-4) compared with controls. Urinary Kidney Injury Molecule-1 levels in stage 2 chronic kidney disease patients were significantly higher than those of the patients with stage 3-4 chronic kidney disease. Urinary Kidney Injury Molecule-1 levels, along with urinary albumin excretion and the duration of diabetes, were found to be independent risk factors associated with low glomerular filtration rates. Conclusion: Urinary Kidney Injury Molecule-1 levels seems to predict renal injury secondary to diabetic nephropathy in early period independent of albuminuria, because urinary Kidney Injury Molecule-1 was elevated despite normal urinary albumin excretion in the normoalbuminuric subgroup. Urinary Kidney Injury Molecule-1 levels, which are elevated in primarily in stage 2, shows a gradual decrease in patients with chronic kidney disease stages 3 and 4; thus, urinary Kidney Injury Molecule-1 levels may be useful in tracking the progression of kidney disease.

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