The progression and complications of chronic kidney disease should differ depending on the cause (C), glomerular filtration rate category (G), and albuminuria (A). The KNOW-CKD (KoreaN Cohort Study for Outcome in Patients With Chronic Kidney Disease), which is a prospective cohort study, enrolls subjects with chronic kidney disease stages 1 to 5 (predialysis). Nine nephrology centers in major university hospitals throughout Korea will enroll approximately 2,450 adults with chronic kidney disease over a 5-year period from 2011 to 2015. The participating individuals will be monitored for approximately 10 years until death or until end-stage renal disease occurs. The subjects will be classified into subgroups based on the following specific causes of chronic kidney disease: glomerulonephritis, diabetic nephropathy, hypertensive nephropathy, polycystic kidney disease, and others. The eligible subjects will be evaluated at baseline for socio-demographic information, detailed personal/family history, office BP, quality of life, and health behaviors. After enrollment in the study, thorough assessments, including laboratory tests, cardiac evaluation and radiologic imaging, will be performed according to the standardized protocol. The biospecimen samples will be collected regularly. A renal event is defined by >50% decrease in estimated GFR (eGFR) from the baseline values, doubling of serum creatinine, or end-stage renal disease. The primary composite outcome consists of renal events, cardiovascular events, and death. As of September 2013, 1,470 adult chronic kidney disease subjects were enrolled in the study, including 543 subjects with glomerulonephritis, 317 with diabetic nephropathy, 294 with hypertensive nephropathy and 249 with polycystic kidney disease. As the first large-scale chronic kidney disease cohort study to be established and maintained longitudinally for up to 10 years, the KNOW-CKD will help to clarify the natural course, complication profiles, and risk factors of Asian populations with chronic kidney disease. No. NCT01630486 at http://www.clinicaltrials.gov .

Kim NH, et al. J Korean Med Sci. 2015 Mar;30(3):272-277. http://dx.doi.org/10.3346/jkms.2015.30.3.272

Hyun YY, et al. J Korean Med Sci. 2017 Feb;32(2):257-263. https://doi.org/10.3346/jkms.2017.32.2.257

Kook-Hwan Oh, Minjung Kang, Eunjeong Kang, Hyunjin Ryu, Seung Hyeok Han, Tae-Hyun Yoo, Soo Wan Kim, Dong-Wan Chae, Kyu-Beck Lee, Sue K. Park, Yeong Hoon Kim, Curie Ahn, for the KNOW-CKD Study Investigators. Kidney Research and Clinical Practice 2020;39:121-35. https://doi.org/10.23876/j.krcp.20.042

Recent studies have showed that epithelial-mesenchymal transition (EMT) is a key process of glomerular and tubulointerstitial pathology in many chronic kidney diseases. However, there are no data of EMT in humane autosomal dominant polycystic kidney disease (ADPKD). ADPKD kidneys (N = 5) with end stage renal disease (ESRD) and control kidneys (N = 4) were analyzed immnunohistochemically. We evaluated α-SMA, E-cadherin, vimentin, TGF-β1 and Smad 2/3 expression in ADPKD and compared them with those in control kidney. These immunohistochemical findings were quantitatively analyzed by computer-assisted image analyzer and positive tubules (%). There were severe interstitial fibrosis and proliferation of α-SMA+ myofibroblasts in ADPKD. Cystic tubular epithelial cells in ADPKD lost epithelial marker (E-cadherin) and expressed mesenchymal markers (α-SMA, vimentin). There were significant increases of α-SMA (34.3 ± 11.7% vs 0.9 ± 1.5%), vimentin (19.9 ± 3.9% vs 3.3 ± 1.4%), TGF-β1 (5.42 ± 2.83% vs 0%) and Smad 2/3 (3.4 ± 1.7% vs 0.7 ± 0.6%) in ADPKD kidneys compared with control kidneys evidenced by computer-assisted image analyzer. When we analyze the positive tubules (%), the results were the same as computer-assisted image analyzer. Our results showed that the end stage of ADPKD is associated with TGF-β, Smad 2/3 and markers of EMT. It suggests that TGF-β mediated EMT has a role in progression of ADPKD.

Dietary net endogenous acid production (NEAP), which represents total dietary load of nonvolatile acid, may affect kidney function. Estimated NEAP (eNEAP) is calculated indirectly by the ratio of protein and potassium intake. A few studies are available assessing the association between eNEAP and chronic kidney disease (CKD), and its relation to dietary protein and potassium intake in the elderly. A total 1,369 community-dwelling elderly Koreans in the Kangbuk Samsung Cohort Study (KSCS) were evaluated using a food frequency questionnaire (FFQ) and comprehensive health examination. We evaluated the association between eNEAP and the CKD. We also examined their relation to protein and potassium intake. eNEAP was correlated with potassium intake (r = -0.410, P < 0.001), but was not correlated with protein intake (r = -0.004, P = 0.879). In a full multivariate adjustment for sociodemographic factors, dietary factors, and comorbidities, the participants with higher eNEAP quartiles (Q2, Q3, Q4) had higher odds of CKD compared to the lowest eNEAP quartile (Q1); OR (95% CI) were 1.47 (0.78–2.72), 1.66 (0.85–3.23), and 2.30 (1.16–4.60) respectively (P for trend = 0.019). The odds of CKD decreased for participants with higher potassium intake quartiles (Q2, Q3, Q4) compared to the lowest potassium intake quartile (Q1); OR (95% CI) were 0.52 (0.28–0.95), 0.50 (0.26–0.96), and 0.50 (0.21–0.99) respectively (P for trend = 0.050). Protein intake was not associated with CKD. The association between eNEAP and CKD was similar in subgroup analysis. Dietary acid load was associated with CKD. Among the nutrients related to dietary acid load, potassium intake was negatively associated with CKD, but protein intake was not associated with CKD in elderly adults.