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Chronic kidney disease

MedGen UID:
473458
Concept ID:
C1561643
Disease or Syndrome
Synonyms: Chronic Kidney Disease; Chronic Kidney Diseases; Chronic Renal Disease; Chronic Renal Diseases; Disease, Chronic Kidney; Disease, Chronic Renal; Diseases, Chronic Kidney; Diseases, Chronic Renal; Kidney Disease, Chronic; Kidney Diseases, Chronic; Renal Disease, Chronic; Renal Diseases, Chronic
SNOMED CT: Chronic kidney disease (709044004); CKD - chronic kidney disease (709044004); Chronic renal disease (709044004)
 
HPO: HP:0012622
Monarch Initiative: MONDO:0005300

Definition

Functional anomaly of the kidney persisting for at least three months. [from HPO]

Conditions with this feature

Primary hypomagnesemia
MedGen UID:
120640
Concept ID:
C0268448
Disease or Syndrome
Familial hypomagnesemia with hypercalciuria and nephrocalcinosis is a progressive renal disorder characterized by excessive urinary Ca(2+) and Mg(2+) excretion. There is progressive loss of kidney function, and in about 50% of cases, the need for renal replacement therapy arises as early as the second decade of life (summary by Muller et al., 2006). Amelogenesis imperfecta may also be present in some patients (Bardet et al., 2016). A similar disorder with renal magnesium wasting, renal failure, and nephrocalcinosis (HOMG5; 248190) is caused by mutations in another tight-junction gene, CLDN19 (610036), and is distinguished by the association of severe ocular involvement. For a discussion of phenotypic and genetic heterogeneity of familial hypomagnesemia, see HOMG1 (602014).
Factor H deficiency
MedGen UID:
96024
Concept ID:
C0398777
Disease or Syndrome
C3 glomerulopathy (C3G) is a complex ultra-rare complement-mediated renal disease caused by uncontrolled activation of the complement alternative pathway (AP) in the fluid phase (as opposed to cell surface) that is rarely inherited in a simple mendelian fashion. C3G affects individuals of all ages, with a median age at diagnosis of 23 years. Individuals with C3G typically present with hematuria, proteinuria, hematuria and proteinuria, acute nephritic syndrome or nephrotic syndrome, and low levels of the complement component C3. Spontaneous remission of C3G is uncommon, and about half of affected individuals develop end-stage renal disease (ESRD) within ten years of diagnosis, occasionally developing the late comorbidity of impaired visual acuity.
X-linked recessive nephrolithiasis with renal failure
MedGen UID:
96047
Concept ID:
C0403720
Disease or Syndrome
X-linked recessive nephrolithiasis with renal failure (XRN) is a form of X-linked hypercalciuric nephrolithiasis, which comprises a group of disorders characterized by proximal renal tubular reabsorptive failure, hypercalciuria, nephrolithiasis, and renal insufficiency. These disorders have also been referred to as the 'Dent disease complex' (Scheinman, 1998; Gambaro et al., 2004). For a general discussion of Dent disease, see 300009.
Cranioectodermal dysplasia 1
MedGen UID:
96586
Concept ID:
C0432235
Disease or Syndrome
Cranioectodermal dysplasia (CED) is a ciliopathy with skeletal involvement (narrow thorax, shortened proximal limbs, syndactyly, polydactyly, brachydactyly), ectodermal features (widely spaced hypoplastic teeth, hypodontia, sparse hair, skin laxity, abnormal nails), joint laxity, growth deficiency, and characteristic facial features (frontal bossing, low-set simple ears, high forehead, telecanthus, epicanthal folds, full cheeks, everted lower lip). Most affected children develop nephronophthisis that often leads to end-stage kidney disease in infancy or childhood, a major cause of morbidity and mortality. Hepatic fibrosis and retinal dystrophy are also observed. Dolichocephaly, often secondary to sagittal craniosynostosis, is a primary manifestation that distinguishes CED from most other ciliopathies. Brain malformations and developmental delay may also occur.
Hypoparathyroidism, deafness, renal disease syndrome
MedGen UID:
374443
Concept ID:
C1840333
Disease or Syndrome
HDR syndrome (HDRS), also known as Barakat syndrome, is a heterogeneous disorder characterized by the triad of Hypoparathyroidism (H), nerve Deafness (D) and/or Renal disease (R). Variable clinical features include hypogonadotrophic hypogonadism, polycystic ovaries, congenital heart disease, retinitis pigmentosa, and cognitive disability (Barakat et al., 2018).
Dent disease type 2
MedGen UID:
336867
Concept ID:
C1845167
Disease or Syndrome
Dent disease, an X-linked disorder of proximal renal tubular dysfunction, is characterized by low molecular weight (LMW) proteinuria, hypercalciuria, and at least one additional finding including nephrocalcinosis, nephrolithiasis, hematuria, hypophosphatemia, chronic kidney disease (CKD), and evidence of X-linked inheritance. Males younger than age ten years may manifest only LMW proteinuria and/or hypercalciuria, which are usually asymptomatic. Thirty to 80% of affected males develop end-stage renal disease (ESRD) between ages 30 and 50 years; in some instances ESRD does not develop until the sixth decade of life or later. The disease may also be accompanied by rickets or osteomalacia, growth restriction, and short stature. Disease severity can vary within the same family. Males with Dent disease 2 (caused by pathogenic variants in OCRL) may also have mild intellectual disability, cataracts, and/or elevated muscle enzymes. Due to random X-chromosome inactivation, some female carriers may manifest hypercalciuria and, rarely, renal calculi and moderate LMW proteinuria. Females rarely develop CKD.
Hypophosphatemic rickets, X-linked recessive
MedGen UID:
335115
Concept ID:
C1845168
Disease or Syndrome
X-linked recessive hypophosphatemic rickets (XLHRR) is a form of X-linked hypercalciuric nephrolithiasis, which comprises a group of disorders characterized by proximal renal tubular reabsorptive failure, hypercalciuria, nephrocalcinosis, and renal insufficiency. These disorders have also been referred to as the 'Dent disease complex' (Scheinman, 1998; Gambaro et al., 2004). For a general discussion of Dent disease, see 300009.
Dent disease type 1
MedGen UID:
336322
Concept ID:
C1848336
Disease or Syndrome
Dent disease, an X-linked disorder of proximal renal tubular dysfunction, is characterized by low molecular weight (LMW) proteinuria, hypercalciuria, and at least one additional finding including nephrocalcinosis, nephrolithiasis, hematuria, hypophosphatemia, chronic kidney disease (CKD), and evidence of X-linked inheritance. Males younger than age ten years may manifest only LMW proteinuria and/or hypercalciuria, which are usually asymptomatic. Thirty to 80% of affected males develop end-stage renal disease (ESRD) between ages 30 and 50 years; in some instances ESRD does not develop until the sixth decade of life or later. The disease may also be accompanied by rickets or osteomalacia, growth restriction, and short stature. Disease severity can vary within the same family. Males with Dent disease 2 (caused by pathogenic variants in OCRL) may also have mild intellectual disability, cataracts, and/or elevated muscle enzymes. Due to random X-chromosome inactivation, some female carriers may manifest hypercalciuria and, rarely, renal calculi and moderate LMW proteinuria. Females rarely develop CKD.
Cryoglobulinemic vasculitis
MedGen UID:
343814
Concept ID:
C1852456
Disease or Syndrome
A rare immune complex-mediated vasculitis characterized by the presence of circulating cryoprecipitable immune complexes in the serum, manifesting clinically with the classical triad of purpura, weakness and arthralgia.
Renal coloboma syndrome
MedGen UID:
339002
Concept ID:
C1852759
Disease or Syndrome
PAX2-related disorder is an autosomal dominant disorder associated with renal and eye abnormalities. The disorder was originally referred to as renal coloboma syndrome and characterized by renal hypodysplasia and abnormalities of the optic nerve; with improved access to molecular testing, a wider range of phenotypes has been recognized in association with pathogenic variants in PAX2. Abnormal renal structure or function is noted in 92% of affected individuals and ophthalmologic abnormalities in 77% of affected individuals. Renal abnormalities can be clinically silent in rare individuals. In most individuals, clinically significant renal insufficiency / renal failure is reported. End-stage renal disease requiring renal transplant is not uncommon. Uric acid nephrolithiasis has been reported. Ophthalmologic abnormalities are typically described as optic nerve coloboma or dysplasia. Iris colobomas have not been reported in any individual with PAX2–related disorder. Ophthalmologic abnormalities may significantly impair vision in some individuals, while others have subtle changes only noted after detailed ophthalmologic examination. Additional clinical findings include high-frequency sensorineural hearing loss, soft skin, and ligamentous laxity. PAX2 pathogenic variants have been identified in multiple sporadic and familial cases of nonsyndromic renal disease including renal hypodysplasia and focal segmental glomerulosclerosis.
Focal segmental glomerulosclerosis 2
MedGen UID:
349053
Concept ID:
C1858915
Disease or Syndrome
Focal segmental glomerulosclerosis (FSGS) is a pathologic entity associated clinically with proteinuria, the nephrotic syndrome (NPHS), and progressive loss of renal function. It is a common cause of end-stage renal disease (ESRD) (review by Meyrier, 2005). For a general phenotypic description and a discussion of genetic heterogeneity of focal segmental glomerulosclerosis and nephrotic syndrome (NPHS), see FSGS1 (603278).
Arteriosclerosis, severe juvenile
MedGen UID:
395330
Concept ID:
C1859725
Disease or Syndrome
RHYNS syndrome
MedGen UID:
356371
Concept ID:
C1865794
Disease or Syndrome
RHYNS syndrome is characterized by gaze palsy, retinitis pigmentosa, sensorineural hearing loss, hypopituitarism, nephronophthisis, and mild skeletal dysplasia (Di Rocco et al., 1997).
Nephropathy, progressive tubulointerstitial, with cholestatic liver disease
MedGen UID:
355562
Concept ID:
C1865831
Disease or Syndrome
Familial juvenile hyperuricemic nephropathy type 2
MedGen UID:
414347
Concept ID:
C2751310
Disease or Syndrome
The two clinical presentations observed in autosomal dominant tubulointerstitial kidney disease – REN (ADTKD-REN) correlate with the renin protein domains affected by the causative REN variants. Childhood/adolescent onset, the more common presentation (caused by REN variants encoding the signal peptide or prosegment domains), is characterized by decreased estimated glomerular filtration rate, acidosis, hyperkalemia, and anemia early in life, followed by slowly progressive chronic kidney disease (CKD) and gout. Adult onset, the less common presentation (caused by REN variants encoding the mature renin peptide), is characterized by gout or mild slowly progressive CKD, beginning in the third decade. Anemia, hyperkalemia, and acidemia do not occur.
Bardet-Biedl syndrome 2
MedGen UID:
422453
Concept ID:
C2936863
Disease or Syndrome
BBS2 is an autosomal recessive ciliopathy characterized by retinal degeneration, polydactyly, renal disease, hypogonadism, obesity, dysmorphic features, and variable degrees of cognitive impairment (Innes et al., 2010). Mutation in the BBS2 gene is the third most frequent cause of BBS, accounting for approximately 8% of cases (Zaghloul and Katsanis, 2009). For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).
Hyperuricemia, pulmonary hypertension, renal failure, alkalosis syndrome
MedGen UID:
462559
Concept ID:
C3151209
Disease or Syndrome
HUPRA syndrome is a severe autosomal recessive multisystem disorder characterized by onset in infancy of progressive renal failure leading to electrolyte imbalances, metabolic alkalosis, pulmonary hypertension, hypotonia, and delayed development. Affected individuals are born prematurely (summary by Belostotsky et al., 2011).
Nephrotic syndrome, type 8
MedGen UID:
815283
Concept ID:
C3808953
Disease or Syndrome
Any nephrotic syndrome in which the cause of the disease is a mutation in the ARHGDIA gene.
Short-rib thoracic dysplasia 10 with or without polydactyly
MedGen UID:
816505
Concept ID:
C3810175
Disease or Syndrome
Short-rib thoracic dysplasia (SRTD) with or without polydactyly refers to a group of autosomal recessive skeletal ciliopathies that are characterized by a constricted thoracic cage, short ribs, shortened tubular bones, and a 'trident' appearance of the acetabular roof. SRTD encompasses Ellis-van Creveld syndrome (EVC) and the disorders previously designated as Jeune syndrome or asphyxiating thoracic dystrophy (ATD), short rib-polydactyly syndrome (SRPS), and Mainzer-Saldino syndrome (MZSDS). Polydactyly is variably present, and there is phenotypic overlap in the various forms of SRTDs, which differ by visceral malformation and metaphyseal appearance. Nonskeletal involvement can include cleft lip/palate as well as anomalies of major organs such as the brain, eye, heart, kidneys, liver, pancreas, intestines, and genitalia. Some forms of SRTD are lethal in the neonatal period due to respiratory insufficiency secondary to a severely restricted thoracic cage, whereas others are compatible with life (summary by Huber and Cormier-Daire, 2012 and Schmidts et al., 2013). There is phenotypic overlap with the cranioectodermal dysplasias (Sensenbrenner syndrome; see CED1, 218330). For a discussion of genetic heterogeneity of short-rib thoracic dysplasia, see SRTD1 (208500).
Au-Kline syndrome
MedGen UID:
900671
Concept ID:
C4225274
Disease or Syndrome
Au-Kline syndrome is characterized by developmental delay and hypotonia with moderate-to-severe intellectual disability, and typical facial features that include long palpebral fissures, ptosis, shallow orbits, large and deeply grooved tongue, broad nose with a wide nasal bridge, and downturned mouth. There is frequently variable autonomic dysfunction (gastrointestinal dysmotility, high pain threshold, heat intolerance, recurrent fevers, abnormal sweating). Congenital heart disease, hydronephrosis, palate abnormalities, and oligodontia are also reported in the majority of affected individuals. Additional complications can include craniosynostosis, feeding difficulty, vision issues, osteopenia, and other skeletal anomalies.
Hyperuricemic nephropathy, familial juvenile type 4
MedGen UID:
934708
Concept ID:
C4310741
Disease or Syndrome
Autosomal dominant tubulointerstitial kidney disease-5 (ADTKD5) is characterized by the onset of progressive chronic renal disease in the first decades of life. Mild hyperuricemia may be present, but gout, hypertension, and proteinuria are usually absent. The disease may be associated with anemia or neutropenia. Some patients may have additional findings, including poor overall growth and impaired cognitive function. Renal biopsy shows tubulointerstitial abnormalities with atrophic tubules and fibrosis; secondary glomerular abnormalities and simple cysts may also be present (summary by Bolar et al., 2016). For a discussion of genetic heterogeneity and revised nomenclature of ADTKD, see ADTKD1 (162000).
Hypotrichosis-lymphedema-telangiectasia-renal defect syndrome
MedGen UID:
1373459
Concept ID:
C4317151
Disease or Syndrome
Hypotrichosis-lymphedema-telangiectasia-renal defect syndrome is an autosomal dominant disorder characterized by these 4 features, which begin in early childhood and are progressive (summary by Moalem et al., 2015).
Vertebral, cardiac, renal, and limb defects syndrome 2
MedGen UID:
1624065
Concept ID:
C4540014
Disease or Syndrome
Vertebral, cardiac, renal, and limb defects syndrome-2 (VCRL2) is an autosomal recessive congenital malformation syndrome characterized by vertebral segmentation abnormalities, congenital cardiac defects, renal defects, and mild distal limb defects. Additional features are variable (summary by Shi et al., 2017). For a discussion of genetic heterogeneity of VCRL, see VCRL1 (617660).
Familial juvenile hyperuricemic nephropathy type 1
MedGen UID:
1645893
Concept ID:
C4551496
Disease or Syndrome
Autosomal dominant tubulointerstitial kidney disease – UMOD (ADTKD-UMOD) is characterized by normal urinalysis and slowly progressive chronic kidney disease (CKD), usually first noted in the teen years and progressing to end-stage renal disease (ESRD) between the third and seventh decades. Hyperuricemia is often present from an early age, and gout (resulting from reduced kidney excretion of uric acid) occurs in the teenage years in about 8% of affected individuals and develops in 55% of affected individuals over time.
Asphyxiating thoracic dystrophy 1
MedGen UID:
1648057
Concept ID:
C4551856
Congenital Abnormality
Short-rib thoracic dysplasia (SRTD) with or without polydactyly refers to a group of autosomal recessive skeletal ciliopathies that are characterized by a constricted thoracic cage, short ribs, shortened tubular bones, and a 'trident' appearance of the acetabular roof. SRTD encompasses Ellis-van Creveld syndrome (EVC) and the disorders previously designated as Jeune syndrome or asphyxiating thoracic dystrophy (ATD), short rib-polydactyly syndrome (SRPS), and Mainzer-Saldino syndrome (MZSDS). Polydactyly is variably present, and there is phenotypic overlap in the various forms of SRTDs, which differ by visceral malformation and metaphyseal appearance. Nonskeletal involvement can include cleft lip/palate as well as anomalies of major organs such as the brain, eye, heart, kidneys, liver, pancreas, intestines, and genitalia. Some forms of SRTD are lethal in the neonatal period due to respiratory insufficiency secondary to a severely restricted thoracic cage, whereas others are compatible with life (summary by Huber and Cormier-Daire, 2012 and Schmidts et al., 2013). There is phenotypic overlap with the cranioectodermal dysplasias (Sensenbrenner syndrome; see CED1, 218330). Genetic Heterogeneity of Asphyxiating Thoracic Dysplasia SRTD1 has been mapped to chromosome 15q13. See also SRTD2 (611263), caused by mutation in the IFT80 gene (611177); SRTD3 (613091), caused by mutation in the DYNC2H1 gene (603297); SRTD4 (613819), caused by mutation in the TTC21B gene (612014); SRTD5 (614376), caused by mutation in the WDR19 gene (608151); SRTD6 (263520), caused by mutation in the NEK1 gene (604588); SRTD7 (614091), caused by mutation in the WDR35 gene (613602); SRTD8 (615503), caused by mutation in the WDR60 gene (615462); SRTD9 (266920), caused by mutation in the IFT140 gene (614620); SRTD10 (615630), caused by mutation in the IFT172 gene (607386); SRTD11 (615633), caused by mutation in the WDR34 gene (613363); SRTD13 (616300), caused by mutation in the CEP120 gene (613446); SRTD14 (616546), caused by mutation in the KIAA0586 gene (610178); SRTD15 (617088), caused by mutation in the DYNC2LI1 gene (617083); SRTD16 (617102), caused by mutation in the IFT52 gene (617094); SRTD17 (617405), caused by mutation in the TCTEX1D2 gene (617353); SRTD18 (617866), caused by mutation in the IFT43 gene (614068); SRTD19 (617895), caused by mutation in the IFT81 gene (605489); SRTD20 (617925), caused by mutation in the INTU gene (610621); and SRTD21 (619479), caused by mutation in the KIAA0753 gene (617112). See also SRTD12 (Beemer-Langer syndrome; 269860).
Renal hypomagnesemia 5 with ocular involvement
MedGen UID:
1648449
Concept ID:
C4721891
Disease or Syndrome
HOMG5 is an autosomal recessive disorder characterized by severe renal magnesium wasting, progressive renal failure, and nephrocalcinosis. Some patients also have severe visual impairment. Amelogenesis imperfecta has been reported in some patients (summary by Konrad et al., 2006 and Yamaguti et al., 2017). For a discussion of genetic heterogeneity of renal hypomagnesemia, see 602014.
DEGCAGS syndrome
MedGen UID:
1794177
Concept ID:
C5561967
Disease or Syndrome
DEGCAGS syndrome is an autosomal recessive syndromic neurodevelopmental disorder characterized by global developmental delay, coarse and dysmorphic facial features, and poor growth and feeding apparent from infancy. Affected individuals have variable systemic manifestations often with significant structural defects of the cardiovascular, genitourinary, gastrointestinal, and/or skeletal systems. Additional features may include sensorineural hearing loss, hypotonia, anemia or pancytopenia, and immunodeficiency with recurrent infections. Death in childhood may occur (summary by Bertoli-Avella et al., 2021).

Professional guidelines

PubMed

Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group
Kidney Int 2024 Apr;105(4S):S117-S314. doi: 10.1016/j.kint.2023.10.018. PMID: 38490803
Arnett DK, Blumenthal RS, Albert MA, Buroker AB, Goldberger ZD, Hahn EJ, Himmelfarb CD, Khera A, Lloyd-Jones D, McEvoy JW, Michos ED, Miedema MD, Muñoz D, Smith SC Jr, Virani SS, Williams KA Sr, Yeboah J, Ziaeian B
Circulation 2019 Sep 10;140(11):e596-e646. Epub 2019 Mar 17 doi: 10.1161/CIR.0000000000000678. PMID: 30879355Free PMC Article
Whelton PK, Carey RM, Aronow WS, Casey DE Jr, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P, Ovbiagele B, Smith SC Jr, Spencer CC, Stafford RS, Taler SJ, Thomas RJ, Williams KA Sr, Williamson JD, Wright JT Jr
Hypertension 2018 Jun;71(6):1269-1324. Epub 2017 Nov 13 doi: 10.1161/HYP.0000000000000066. PMID: 29133354

Curated

UK NICE Guideline NG238, Cardiovascular disease: risk assessment and reduction, including lipid modification, 2023

UK NICE Guidance, Clinical Guideline CG181, Cardiovascular disease: risk assessment and reduction, including lipid modification, 2023

UK NICE Guideline NG203, Chronic kidney disease: assessment and management, 2021

Recent clinical studies

Etiology

De Bhailis ÁM, Kalra PA
Br J Hosp Med (Lond) 2022 May 2;83(5):1-11. Epub 2022 May 27 doi: 10.12968/hmed.2021.0440. PMID: 35653320
Charles C, Ferris AH
Prim Care 2020 Dec;47(4):585-595. Epub 2020 Sep 25 doi: 10.1016/j.pop.2020.08.001. PMID: 33121630
Lv JC, Zhang LX
Adv Exp Med Biol 2019;1165:3-15. doi: 10.1007/978-981-13-8871-2_1. PMID: 31399958
Gansevoort RT, Correa-Rotter R, Hemmelgarn BR, Jafar TH, Heerspink HJ, Mann JF, Matsushita K, Wen CP
Lancet 2013 Jul 27;382(9889):339-52. Epub 2013 May 31 doi: 10.1016/S0140-6736(13)60595-4. PMID: 23727170
Levey AS, Coresh J
Lancet 2012 Jan 14;379(9811):165-80. Epub 2011 Aug 15 doi: 10.1016/S0140-6736(11)60178-5. PMID: 21840587

Diagnosis

Inker LA, Titan S
Am J Kidney Dis 2021 Nov;78(5):736-749. Epub 2021 Sep 11 doi: 10.1053/j.ajkd.2021.04.016. PMID: 34518032
Charles C, Ferris AH
Prim Care 2020 Dec;47(4):585-595. Epub 2020 Sep 25 doi: 10.1016/j.pop.2020.08.001. PMID: 33121630
Delles C, Vanholder R
Clin Sci (Lond) 2017 Feb 1;131(3):225-226. doi: 10.1042/CS20160624. PMID: 28057893
Zhang L, Wang F, Wang L, Wang W, Liu B, Liu J, Chen M, He Q, Liao Y, Yu X, Chen N, Zhang JE, Hu Z, Liu F, Hong D, Ma L, Liu H, Zhou X, Chen J, Pan L, Chen W, Wang W, Li X, Wang H
Lancet 2012 Mar 3;379(9818):815-22. doi: 10.1016/S0140-6736(12)60033-6. PMID: 22386035
Levey AS, Coresh J
Lancet 2012 Jan 14;379(9811):165-80. Epub 2011 Aug 15 doi: 10.1016/S0140-6736(11)60178-5. PMID: 21840587

Therapy

Kalhan AC, Wong ML, Allen F, Gao X
Ann Acad Med Singap 2022 Sep;51(9):567-574. doi: 10.47102/annals-acadmedsg.2021503. PMID: 36189701
Zheng J, Zhang Y, Rasheed H, Walker V, Sugawara Y, Li J, Leng Y, Elsworth B, Wootton RE, Fang S, Yang Q, Burgess S, Haycock PC, Borges MC, Cho Y, Carnegie R, Howell A, Robinson J, Thomas LF, Brumpton BM, Hveem K, Hallan S, Franceschini N, Morris AP, Köttgen A, Pattaro C, Wuttke M, Yamamoto M, Kashihara N, Akiyama M, Kanai M, Matsuda K, Kamatani Y, Okada Y, Walters R, Millwood IY, Chen Z, Davey Smith G, Barbour S, Yu C, Åsvold BO, Zhang H, Gaunt TR
Int J Epidemiol 2022 Jan 6;50(6):1995-2010. Epub 2021 Oct 20 doi: 10.1093/ije/dyab203. PMID: 34999880Free PMC Article
Yamazaki T, Mimura I, Tanaka T, Nangaku M
Diabetes Metab J 2021 Jan;45(1):11-26. Epub 2021 Jan 22 doi: 10.4093/dmj.2020.0217. PMID: 33508907Free PMC Article
Mallamaci F, Pisano A, Tripepi G
Nephrol Dial Transplant 2020 Mar 1;35(Suppl 2):ii18-ii22. doi: 10.1093/ndt/gfaa012. PMID: 32162664Free PMC Article
Heerspink HJ, Perkins BA, Fitchett DH, Husain M, Cherney DZ
Circulation 2016 Sep 6;134(10):752-72. Epub 2016 Jul 28 doi: 10.1161/CIRCULATIONAHA.116.021887. PMID: 27470878

Prognosis

Wu G, Cai M, Wang C, Zou H, Wang X, Hua J, Lin H
Sci Total Environ 2023 Jul 10;881:163406. Epub 2023 Apr 11 doi: 10.1016/j.scitotenv.2023.163406. PMID: 37054795
Deng Y, Li N, Wu Y, Wang M, Yang S, Zheng Y, Deng X, Xiang D, Zhu Y, Xu P, Zhai Z, Zhang D, Dai Z, Gao J
Front Endocrinol (Lausanne) 2021;12:672350. Epub 2021 Jul 1 doi: 10.3389/fendo.2021.672350. PMID: 34276558Free PMC Article
Guzon-Illescas O, Perez Fernandez E, Crespí Villarias N, Quirós Donate FJ, Peña M, Alonso-Blas C, García-Vadillo A, Mazzucchelli R
J Orthop Surg Res 2019 Jul 4;14(1):203. doi: 10.1186/s13018-019-1226-6. PMID: 31272470Free PMC Article
Chioncel O, Lainscak M, Seferovic PM, Anker SD, Crespo-Leiro MG, Harjola VP, Parissis J, Laroche C, Piepoli MF, Fonseca C, Mebazaa A, Lund L, Ambrosio GA, Coats AJ, Ferrari R, Ruschitzka F, Maggioni AP, Filippatos G
Eur J Heart Fail 2017 Dec;19(12):1574-1585. Epub 2017 Apr 6 doi: 10.1002/ejhf.813. PMID: 28386917
Misurac J
Semin Fetal Neonatal Med 2017 Apr;22(2):98-103. Epub 2016 Oct 10 doi: 10.1016/j.siny.2016.09.003. PMID: 27733241

Clinical prediction guides

Hatta W, Tsuji Y, Yoshio T, Kakushima N, Hoteya S, Doyama H, Nagami Y, Hikichi T, Kobayashi M, Morita Y, Sumiyoshi T, Iguchi M, Tomida H, Inoue T, Koike T, Mikami T, Hasatani K, Nishikawa J, Matsumura T, Nebiki H, Nakamatsu D, Ohnita K, Suzuki H, Ueyama H, Hayashi Y, Sugimoto M, Yamaguchi S, Michida T, Yada T, Asahina Y, Narasaka T, Kuribasyashi S, Kiyotoki S, Mabe K, Nakamura T, Nakaya N, Fujishiro M, Masamune A
Gut 2021 Mar;70(3):476-484. Epub 2020 Jun 4 doi: 10.1136/gutjnl-2019-319926. PMID: 32499390Free PMC Article
Mihai S, Codrici E, Popescu ID, Enciu AM, Albulescu L, Necula LG, Mambet C, Anton G, Tanase C
J Immunol Res 2018;2018:2180373. Epub 2018 Sep 6 doi: 10.1155/2018/2180373. PMID: 30271792Free PMC Article
Bosevski M
Pril (Makedon Akad Nauk Umet Odd Med Nauki) 2017 Sep 1;38(2):29-33. doi: 10.1515/prilozi-2017-0019. PMID: 28991768
Glassock RJ, Denic A, Rule AD
J Nephrol 2017 Aug;30(4):477-483. Epub 2016 Nov 25 doi: 10.1007/s40620-016-0362-x. PMID: 27885585
Tonelli M, Riella M
Am J Hypertens 2014 Mar;27(3):287-90. doi: 10.1093/ajh/hpt284. PMID: 24503459

Recent systematic reviews

Garcia Sanchez JJ, Thompson J, Scott DA, Evans R, Rao N, Sörstadius E, James G, Nolan S, Wittbrodt ET, Abdul Sultan A, Stefansson BV, Jackson D, Abrams KR
Adv Ther 2022 Jan;39(1):193-220. Epub 2021 Dec 8 doi: 10.1007/s12325-021-02006-z. PMID: 34881414Free PMC Article
Al Khalaf S, Bodunde E, Maher GM, O'Reilly ÉJ, McCarthy FP, O'Shaughnessy MM, O'Neill SM, Khashan AS
Am J Obstet Gynecol 2022 May;226(5):656-670.e32. Epub 2021 Nov 2 doi: 10.1016/j.ajog.2021.10.037. PMID: 34736915
Villanego F, Naranjo J, Vigara LA, Cazorla JM, Montero ME, García T, Torrado J, Mazuecos A
Nefrologia (Engl Ed) 2020 May-Jun;40(3):237-252. Epub 2020 Apr 15 doi: 10.1016/j.nefro.2020.01.002. PMID: 32305232
Spoto B, Pisano A, Zoccali C
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    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.
    • Bookshelf
      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Curated

    • NICE, 2023
      UK NICE Guideline NG238, Cardiovascular disease: risk assessment and reduction, including lipid modification, 2023
    • NICE, 2023
      UK NICE Guidance, Clinical Guideline CG181, Cardiovascular disease: risk assessment and reduction, including lipid modification, 2023
    • NICE, 2021
      UK NICE Guideline NG203, Chronic kidney disease: assessment and management, 2021

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