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Description : This medical presentation titled ""HIV and Kidney Disease"" tells us why kidney disease a problem in HIV, provides types of Renal Disease and medications.

Tags : HIV, Kidney Disease, Renal Disease, medications, infection, Nephropathy, HIVAN, Human Immunodeficiency Virus, HIV, infection, cells, immune system, AIDS, Acquired Immune Deficiency Syndrome, HIV Positive

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HIV and Kidney Disease Epidemiology Types of Renal Disease Medications Brad Canada, MD 1
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Epidemiology Why is Kidney Disease a Problem in HIV?
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Highly Active Antiretroviral Therapy Improves Survival of HIV-Infected Hemodialysis Patient 3 Am J Kidney Dis. 2000 Sep;36(3):574-80.
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Deaths from HIV in the United States Selik RM, et al. J Acquir Immune Defic Syndr. 2002;29(4):378-387. * * * * * * * * * * * * * Dementia/ Encephalopathy Acute Pancreatitis 0 1 2 3 4 5 6 7 8 9 10 Percentage Year 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 Wasting/Cachexia Heart Disease (other than Cardiac Arrest) Kidney Disease Liver Disease other than Viral Hepatitis * Kidney Disease
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Causes of ESRD in African Americans (1993-1997) Diabetes Hypertension HIV Related Focal GN SLE nephritis Membranous HUS Amyloidosis Postinfectious GN African Americans aged 20-65 years (n=66,063) 0 10,000 20,000 30,000 24,535 20,748 3168 2186 1703 315 96 90 34 GN=glomerulonephritis; HUS=hemolytic anemia syndrome. Monahan M, et al. Semin Nephrol. 2001;21(4):394-402.
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Schwartz, et al JASN 16: 2412-2420, 2005
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Relative Hazard of Death Before the Widespread Use of ARTa, According to Absolute CD4 Cell Count for Women With or Without Proteinuriab WIHS: Mortality in HIV+ Women With and Without Proteinuria Prior to Widespread ART Use aDefined as October 31, 1997. bThe baseline hazard ratio was 1 for women without proteinuria who had a CD4 cell count of 350 cells/mm3. Szczech LA, et al. Clin Infect Dis. 2004;39:1199-1206. 7
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WIHS: Association Between Renal Disease and Outcomes Among HIV+ Women Receiving or Not Receiving ART Time (days) Time (days) Proportion of Patients, % Proportion of Patients, % With proteinuria Without proteinuria Szczech LA, et al. Clin Infect Dis. 2004;39:1199-1206. Time to Death Prior to Widespread Use of ARTa Time to AIDS-Defining Illness Prior to Widespread Use of ARTa Time to AIDS-Defining Illness After ART Initation Time to Death After ART Initiation 8 aDefined as October 31, 1997.
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P < 0.0001 P = 0.003 Szczech LA, et al. Clin Infect Dis. 2004;39:1199-1206. Predictors of Mortality in Women with HIV following HAART Initiation Hazard Ratio (95% CI) CD4 Lymphocyte Count Prior History of AIDS-Defining Illness
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Chronic kidney disease in HIV infection: an urban epidemic. 10 AIDS. 2007 Oct 1;21(15):2101-3.
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11 Am J Kidney Dis Am J Kidney Dis 2010; 56:872–882; 56:872–882 Unadjusted 5-year mortality rates in human immunodeficiency virus (HIV)-infected participants stratified by the presence of decreased serum creatinine–based estimated glomerular filtration rate (FRAM, 922,877) all Normal Creat based eGFR
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12 JAIDS Volume 41(2), 1 February 2006, pp 194-200
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13 AIDS. 24(3):387-394, January 28, 2010.
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Time to All-Cause Death P <.0001 for all three HRs. Time to AIDS Death Survival Function % Survival Function % 70 80 90 100 0 100 200 300 400 500 600 700 800 900 1000 70 80 90 100 0 100 200 300 400 500 600 700 800 900 1000 WIHS: Microalbuminuria Is Associated With All-Cause and AIDS Mortality in HIV+ Women No albuminuria (reference) Unconfirmed albuminuria (HR: 3.4, 95% CI: 2.2-5.2) Confirmed microalbuminuria (HR: 3.9, 95% CI: 2.1-7.0) Confirmed proteinuria (HR: 5.8, 95% CI: 3.4-9.8) No albuminuria (reference) Unconfirmed albuminuria (HR: 3.5, 95% CI: 2.2-5.8) Confirmed microalbuminuria (HR: 4.5, 95% CI: 2.3-8.6) Confirmed proteinuria (HR: 5.2, 95% CI: 2.7-10.0) P <.0001 for all three HRs. Wyatt CM, et al. J Acquir Immune Defic Syndr. 2010 Jan 21 [Epub ahead of print]. 14
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© 2010 Lippincott Williams & Wilkins, Inc. Published by Lippincott Williams & Wilkins, Inc. 2 Impact of CKD at Initiation of ART on Mortality The Impact of Kidney Function at Highly Active Antiretroviral Therapy Initiation on Mortality in HIV-Infected Women. Estrella, Michelle; M MD, MHS; Parekh, Rulan; S MD, MS; Abraham, Alison; Astor, Brad; C PhD, MPH; Szczech, Lynda; A MD, MSCE; Anastos, Kathryn; Dehovitz, Jack; A MD, MPH; Merenstein, Daniel; Pearce, C; Leigh MPH, PhD; Tien, Phyllis; Cohen, Mardge; Gange, Stephen JAIDS Journal of Acquired Immune Deficiency Syndromes. 55(2):217-220, October 1, 2010. DOI: 10.1097/QAI.0b013e3181e674f4 TABLE 2 . Hazard Ratios of Mortality Associated With CKD at HAART Initiation WIHS
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VA Cohort: Decreased Kidney Function, Albuminuria and CV Risk aDemographic-adjusted models control for age, sex, and race. Multivariate-adjusted models control for age, sex, race, and time-updated hypertension, diabetes mellitus, chronic obstructive lung disease, dyslipidemia, smoking, CD4 count, HIV VL, ART. b”Normal” defined as albuminuria level 0 mg/dL with an eGFR ≥60 mL/min/1.73m2. cAtherosclerotic CV event: composite outcome of coronary, cerebrovascular, and peripheral arterial disease. Choi AI, et al. Circulation. 2010;121:651-658. 16
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VA Cohort: Association Between Decreased GFR, Albuminuria and CVD Risk in HIV+ Patients 17,264 HIV+ persons receiving care in the VA for Incident CVD, defined as coronary, cerebrovascular, or peripheral arterial disease, and Incident heart failure 7% of patients had reduced kidney function (eGFR <60 mL/min per 1.73 m2) at study entry Choi AI, et al. Circulation. 2010;121:651-658. Atherosclerotic CV Events (per 1000 P-Y) Incidence of Atherosclerotic CV Eventsa in VA Cohort aStratified by eGFR and dipstick albuminuria level. 17
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Types of Renal diseases seen with HIV
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Causes of CKD Non-HIV related Hypertension Diabetes mellitus Non-diabetic glomerular disease Cystic kidney disease Tubulointerstitial disease Co-infection with HBV, HCV, or syphilis HIV-related HIV-Associated Nephropathy (HIVAN) Glomerulopathies, e.g., immune complex glomerulonephritis, IgA glomerulonephritis, membranous glomerulopathy, etc. ART or OI medications http://www.kidney.org/professionals/KLS/aboutCKD.cfm. Kimmel P, et al. Ann Int Med. 2003; 139:214-226. Gupta SK, et al. Clin Infect Dis. 2005; 40:1559-1585.
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HIV-Associated Nephropathy: HIVAN A Disease of Racial Disparity
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Kimmel PL, et al. Ann Intern Med. 2003;139(3):214-226. HIVAN Pathophysiology Podocyte Dysregulation Tubular Epithelial Cell Dysregulation Tubular Degeneration and Regeneration and Microcyst Formation Capillary Loop Collapse HIV-1
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HIVAN 23
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Electron Microscopy of HIVAN 24
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Host factors leading to HIVAN Host Specific genes MYH9 Gene on chromosome 22 that encodes APOL1 protein Renin Angiotensin System NOTCH signaling pathway activated leading to podocyte dysregulation 25
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Genetic Component of CKD: MyH9 Polymorphism MyH9 gene encodes the nonmuscle myosin heavy chain IIA and is expressed in the foot processes of specialized cells of the glomerulus (podocytes) involved in filtration and regulation of GFR Presence of a polymorphism in the MyH9 gene is strongly associated with an increased risk of kidney disease Polymorphism present more frequently in African Americans compared to Caucasian patients May account for the increased risk of CKD among African Americans vs other ethnicities 26 Kopp JB, et al. Nature Gen. 2008;40:1175-1184. Somlo S and Mundel P. Nature Gen. 2000;24:333-335.. Normal GBM Major processes Foot processes Filtration slits
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HIVAN – Major Features Typically heavy proteinuria Typically viral load detectable Usually low CD4 count Definitive diagnosis only by biopsy Large percentage not hypertensive
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(A) Kaplan–Meier estimate of renal survival in two groups of study patients (treated and not treated with ART). Atta M G et al. Nephrol. Dial. Transplant. 2006;21:2809-2813 © The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
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Kaplan–Meier estimates of renal survival in patients with complete and partial virological suppression. Atta M G et al. Nephrol. Dial. Transplant. 2006;21:2809-2813 © The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
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HAART and HIVAN Incidence 12-Year Cohort Study No AIDS AIDS Cases per 1000 person-years 0 5 10 15 20 25 30 35 40 45 Lucas GM, et al. AIDS. 2004;20:18(3):541-546. Numbers in bars represent point estimates for HIV-associated nephropathy incidence in cases per 1000 person-years. Brackets above bars represent upper limits of 95% confidence intervals. No Antiretroviral Therapy Nucleoside Reverse Transcriptase Inhibitor Therapy Highly Active Antiretroviral Therapy Presumed HIV-Associated Nephropathy Incidence Stratified by AIDS Status and Antiretroviral Use 2.6 5.0 26.3 14.4 6.8 0.0 Risk of HIVAN low in patients without AIDS NO HIVAN when HAART used without AIDS occurrence Lower HIVAN associated with NRTI and HAART use compared with no ART in patients with AIDS (p < 0.001 for trend)
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HIV Medications and Renal Related issues
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Current Therapy include a minimum of three active agents Presently licensed drug classes: nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) ** non-nucleoside reverse transcriptase inhibitors (NNRTIs) protease inhibitors (PIs) CCR5 inhibitors integrase inhibitors fusion inibitors 33 **most NRTI’s require dose adjustment for decreased renal function
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Indinavir Precipitates as drug crystals in the urine Volume depletion with sluggish urine flow is most important risk factor Reduced GFR also risk factor Use of medication has declined Other drugs: acyclovir, atazanavir, ciprofloxacin 35
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Light Microscopy of Urinary Sediment A. Rectangular plates of various sizes containing needle-shaped crystals. The plates have irregular borders with occasional tapering and present an internal layering more evident in the largest forms (large arrows). Many crystal fragments are seen in the background; small, triangular pieces (small arrows) represent broken ends of the needles. B. The frequent, typical configuration of indinavir crystals in a sheaf of numerous densely packed needles. C. Several indinavir crystal groupings arranged in a rosette.
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Indinavir Renal Biopsy Light Microscopy Three tubules containing abundant clear intraluminal crystals with needle and rod shapes surrounded by mononuclear cells and giant cells. Adjacent interstitial contains a dense infiltrate on mononuclear leukocytes. High power view with clear intratubular crystals engulfed by intraluminal giant cells.
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Tenofovir-associated Renal Toxicity Clinical Controversy
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Tenofovir (TDF) Toxicity Is it real? How prevalent? Does it matter how you define it? Does it matter how it is measured? Is it clinical trials vs. real world? Patient population Dose adjustment
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TENOFOVIR Tenofovir closely related to adefovir Adefovir is a well described nephrotoxin Tenofovir freely filtered; also secreted by proximal tubule Nephrotoxicity vigilance in clinical trials Adefovir Tenofovir TDF Blood Lumen OAT1 MRP Proximal Tubule
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No Nephrotoxicity No Nephrotoxicity TENOFOVIR Clinical Trials Squires K, et al. Ann Intern Med. 2003;139:313-320. January 2006 No Reported Nephrotoxicity
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Change in GFR (MDRD vs. Cockcroft-Gault) a. Modification of Diet in Renal Disease Equation b. p < 0.001 for difference between baseline and week 48 c. p = 0.010 for difference between baseline and week 48 Enejosa J, et al. 14th CAHR. Vancouver, Canada 2005. Abstract #293P. Gallant JE, et al. The New England Journal of Medicine 2006;354(3):251-260. Estimated by MDRDa Estimated by Cockcroft-Gault a. p = 0.660 for difference between baseline and week 48 b. p < 0.001 for difference between baseline and week 48 Results through Week 48 Results through Week 48 †Not co-formulated as Truvada †Not co-formulated as Truvada RCT of treatment-naïve patients comparing AZT/3TC/EFV with TDF/FTC/EFV over 48 weeks Weight increased by 2.1 kg (TDF-FTC) vs. 1.1 kg (CBV) No graded abnormalities in serum phosphorus, creatinine No cases of Fanconi Syndrome observed Gilead 934 study
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Reported Incidence of TDF Nephrotoxicity in Clinical Use Harris M, et al. 2nd IAS. Paris, France 2003. Abstract #730. Reynes J, et al. 10th CROI. Boston, MA 2003. Abstract #717. Karras A, et al. Clin Infect Diseases. 2003;36(8):1070-1073. Padilla S, et. al. AIDS Patient Care and STDs. 2005;19(7):421-424. Explanation of Variation in Incidence: Surveillance and recognition biases Lack of a standard definition Reported findings: mean vs. median Risk in retrospective database studies1-6 Jones R, et al. J Acquir Immune Defic Syndr. 2004;37(4):1489-1495. Nelson M, et al. 13th CROI. Denver, CO 2006. Abstract #781.
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120 100 80 60 40 20 0 0 90 180 270 360 Days CRCL * * * Median CRCL Over Time for TDF and Other-NRTI *P < 0.05 Change from Baseline for TDF vs. NRTI Published Johns Hopkins Cohort Adapted from Gallant JE, et al. Clin Infect Dis. 2005;40(8):1194-1198. Gallant JE, et al. 12th CROI. Boston, MA 2005. Poster #820. # on TDF 344 344 316 241 185 # on NRTI 314 314 294 235 190
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What Are Possible Risk Factors for TDF Renal Failure? Potential risk factors Lower baseline renal function Not only just high serum creatinine1 Lower weight2 Lower CD4 count3 RTV-boosted PI and didanosine use4 Previous adefovir toxicity Duration of TDF use Race Other nephrotoxins Harris M, et al. 11th CROI. San Francisco, CA 2004. Abstract #750. Peyriere H, et al. J Acquir Immune Defic Syndr. 2004;35:269-273. Harris M, et al. 2nd IAS. 2003. Abstract #730 and Gallant J, et al. Clin Infect Dis. 2005;40:1194-1198. Zimmermann AE, et al. Clin Infect Dis. 2006;42(2):283-290.
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Fanconi Syndrome Drug-specific Renal Disease
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Fanconi Syndrome Hypophosphatemia, acidosis, glycosuria, aminoaciduria, hypokalemia = FANCONI SYNDROME X X X Phosphate Proximal Tubule Cell Introduction of Nephrotoxic Agent
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Tenofovir-induced Fanconi Syndrome Mean (range) unless otherwise specified Pooled from: Peyriere H, et al. J Acquir Immune Defic Syndr. 2004;35:269-273. Rifkin BS, Perazella MA. Am J Med. 2004;117(4):282-284. Karras A, et al. Clin Infect Diseases. 2003;36(8):1070-1073. Rollot F, et al. Clin Infect Dis. 2003;37(12):e174-e176. Saumoy M, et al. AIDS. 2004;18(12):1741-1749. Gaspar G, et al. AIDS. 2004;18:351-352. Literature Review of 25 Currently Published Cases
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Characteristics of TDF-induced Fanconi Syndrome Mean (range) unless otherwise specified Pooled from: Peyriere H, et al. J Acquir Immune Defic Syndr. 2004;35:269-273. Rifkin BS, Perazella MA. Am J Med. 2004;117(4):282-284. Karras A, et al. Clin Infect Diseases. 2003;36(8):1070-1073. Rollot F, et al. Clin Infect Dis. 2003;37(12):e174-e176. Saumoy M, et al. AIDS. 2004;18(12):1741-1749. Gaspar G, et al. AIDS. 2004;18:351-352.
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Withdrawal of Drug as Management of Tenofovir-induced Fanconi Syndrome Discontinuation of TDF resulted in: Electrolyte abnormalities resolved Glycosuria resolved Proteinuria partially resolved (no baseline data) Biopsy findings reveal proximal ATN No glomerular, vascular, or interstitial changes
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ppt slide no 51 content not found
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“Gilead posts higher profit, seeks Quad approval” Reuters Oct 27, 2011
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The Quad contains four Gilead compounds in a fixed-dose, single-tablet: Elvitegravir (Integrase inhibitor) Cobicistat, a pharmacoenhancing or "boosting" agent Emtricitabine Tenofovir Quad Pill 53
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54 Proximal Tubule Blood (Basolateral) Urine (Apical) Active Tubular Secretion Creatinine Dolutegravir Cimetidine Trimethoprim Ritonavir Cobicistat ATP ATP ATP OCT2 Lepist E-I, et al. ICAAC 2011. Chicago. # A1-1724 Cobicistat and Ritonavir Inhibition of Creatinine by OCT2 and MATE1 transporters
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55 German P, et al. ICAAC 2011. Chicago. # H2-804 Evaluation of potential effect of COBI on renal function comparing actual GFR (aGFR) to estimated GFR (eGFR) in 2 cohorts with normal renal function and mild-moderate impairment Methods Comparison of estimated GFR to actual GFR using iohexol* *Probe drug excreted almost exclusively by glomerular filtration; iohexol 1500 mg IV bolus over 1-2 minutes Cobicistat: GFR Changes in Normal and Impaired Renal Function Methods Day 7 Day14 Cohort 2 Impaired Renal Function (eGFR 50 to 79 mL/min) N=18 COBI Follow up Cohort 1 Normal Renal Function (eGFR ≥ 80 mL/min)) N=36 COBI+RTV Placebo Placebo Follow up RTV+COBI Placebo n= 12 n= 12 n= 12
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56 Normal renal function: eGFR ≥ 80 mL/min; Mild-moderate: eGFR 50 to 79 mL/min *p-values comparison between treatment groups for change from baseline to day 7 COBI effects were seen in estimated GFR but not actual GFR Onset was within days of initiation and quickly reversed upon COBI discontinuation The time to onset, magnitude, and time to resolution of changes in estimated GFR are consistent with altered proximal tubular secretion of creatinine thru inhibition of drug transporters German P, et al. ICAAC 2011. Chicago. # H2-804 Cobicistat: GFR Changes in Normal and Impaired Renal Function Results by Cockcroft-Gault Normal Renal Function Mild-Moderate Impairment *p < 0.05 Day COBI No COBI *p < 0.05 Day COBI No COBI
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57 Cobicistat and Ritonavir Proximal Renal Tubular Cell Uptake and Efflux Transporters Methods Inhibition of OCT2, OCTN1, MATE1, MATE2-K, Pgp, MRP2 and BCRP transporters was studied in transfected cell-lines Known inhibitors were used as positive controls in each independent assay Studies were conducted with drugs known to reduce eGFR including cimetidine, trimethoprim, dolutegravir (DTG), COBI and RTV Conclusions: Inhibition of the active tubular secretion of creatinine may explain the effects of these agents on Cr and its impact on eGFR Uptake from plasma into the proximal tubule by OCT2 (DTG) Efflux into the urine by MATE1 (cimetidine, trimethoprim, COBI and RTV) Lepist E-I, et al. ICAAC 2011. Chicago. # A1-1724
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IDSA Guidelines: Screening Algorithm Qualitative assessment for risk of kidney disease Race Family history of kidney disease CD4 lymphocyte count HIV RNA level History of use of nephrotoxic medications Comorbidities Diabetes mellitus Hypertension Hepatitis C infection Screening studies for patients at increased risk: Urine analysis (for proteinuria) Serum creatinine (estimate creatinine clearance or glomerular filtration rate using appropriate formula) Abnormal values > +1 proteinuria by dipstick creatinine clearance or glomerular filtration rate < 60 mL/min/1.73 m2 No abnormal values Evaluate proteinuria further with spot urine to protein creatinine Renal ultrasound Consider referral to a nephrologist for further evaluation and potentially biopsy Groups at risk for kidney disease related to HIV infection should be reassessed periodically (e.g., yearly) Groups without risk factors for kidney disease should be followed clinically and reassessed based on the occurrence of signs and symptoms or as clinical events dictate Gupta S, et al. Clin Infect Dis. 2005; 40(11):1559-1585.
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Acute Kidney Injury AKI is an important and common problem in HIV-infected patients Prevention and early treatment of AKI is possible Knowledge of underlying risk factors Diverse etiologies (some unique) cause AKI in these patients Underlying disease states predispose to AKI Perazella MA. Am J Med Sci. 2000;319(6):385-391.
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Etiology of Acute Renal Failure Franceschini N, et al. Kidney Int. 2005;67(4):1526-1531. 10 22 9 6 2 5 2 11 2 2 1 1 2 1 18 17 0 10 20 30 40 50 Pre-renal Renal Obstructive Unknown Diarrhea, Nausea, Vomiting, Dehydration Heart Failure Cirrhosis Pancreatitis Adrenal Insufficiency Sepsis or Infection Erythroderma 43 (38%) 48 (46%) 9 (7%) 11 (9%) Acute Tubular Necrosis, Ischemic Nephrotoxic Drugs Nephrotoxic Radiocontrast Interstitial Nephritis Thrombotic Thrombocytopenic Purpurahemolytic Uremic Syndrome Kidney Stones Crystalluria Gross Hematuria ARF Events Number Causes
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Acute Interstitial Nephritis Rossert J. Kidney Int. 2001;60(2):804-817. Renal Failure Dialysis Hematuria Gross Hematuria Pyuria Proteinuria Extrarenal Symptoms Eosinophilia 50% 100% 50% 100% Methicillin Other Antibiotics
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Acute Interstitial Nephritis Prevention and Treatment Prevention of AIN: Idiosyncratic reaction that is not dose-dependent and can occur quickly with reintroduction of a drug Avoid use of drugs in patients with known allergy Closely monitor HIV patients given high-risk drugs Sulfas Rifampin Treatment of AIN: Early diagnosis avoids tubulointerstitial fibrosis and permanent renal insufficiency Withdraw the culprit medication Consider corticosteroids* if renal function does not improve within 1 week to 10 days Perazella MA. Am J Med Sci. 2000;319(6):385-391. *May want to avoid in severe infection
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Renal 101 What are the Considerations and Risks?
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30 mg Microalbuminuria and Proteinuria: Key Thresholds < 300 mg microalbuminuria
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Serum Creatinine (mg/dL) GFR versus Serum Creatinine Available at: http//medical.dictionary.thefreedictionary.com/. Accessed on March 1, 2005. Johnson R, et al. Comprehensive Clinical Nephrology. 2000. Mosby. St. Louis. 4.15.1–4.15.15. 9.0 8.0 7.0 6.0 5.0 4.0 3.0 2.0 1.0 0.0 0 20 40 60 80 100 120 140 160 180 Inulin Clearance (mL/min/1.73 m2) GFR versus Serum Creatinine
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GFR Equations Compared 6 variable: Cr, BUN, age, alb, race, sex 4 variable: Cr, age, race, sex Levey AS, et al. Ann Intern Med. 1999;130(6):461-470 Levey AS. et al. J Am Soc Neph. 2000; 11: 155A (Abstract) Cockcroft-Gault MDRD [140 - age] x weight (kg) [72 x PCr] x (0.85 if female) 186.3 x PCr –1.154 x age –0.203 x (0.742 if female) (1.212 if black) x
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Kidney Function as Estimated Using the MDRD Formula 0 20 40 60 80 100 120 1 2 3 4 5 6 7 8 9 10 11 Serum Creatinine (mg/dL) eGFR (mL/min) 30-yr-old Black Male 55-yr-old Black Male 55-yr-old White Male 55-yr-old White Female
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GFR: mL/min/1.73 m2 *May be normal for age K/DOQI Guidelines, National Kidney Foundation. Available at: http://www.kidney.org/professionals/kdoqi/guidelines_ckd/p4_class_g1.htm. Accessed March 7, 2006. National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) Classification of Chronic Kidney Disease Chronic kidney disease is defined as either kidney damage or GFR <60 mL/min/1.73 m2 for ≤ 3 months. Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.