Chronic renal failure medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]


Treatment is aimed at specific causes of chronic renal failure. It includes optimized glucose levels in patients with diabetes, management of blood pressure, immunomodulators for glomerulonephritis, emerging specific therapies to retard cytogenesis in polycystic kidney disease and replacement of critical hormones and chemicals produced and utilized by normally healthy kidneys. Any acceleration in the disease process should prompt a search for superimposed acute or subacute disease process that is potentially reversible. These include extravascular fluid volume depletion, urinary tract infection, obstructive uropathy, exposure to nephrotoxic agents such as NSAIDS or radiocontrasts, re-activation and flare of the primary disease like SLE or vasculitis.

Medical Therapy

Management plan

GFR in ml/min per 1.73 m² Management plan
> or equal to 90 Diagnosis and treatment, treatment of comorbid conditions, slow progression of the disease process, cardiovascular disease risk reduction
60-89 Estimate disease progression
30-59 Evaluate and treat complications
15-29 Preparation for renal replacement therapy
<15 (or dialysis) Kidney replacement (with symptoms of uremia)

Blood pressure management

Control of blood glucose

  • Tight glycemic control reduces the risk of progression of diabetic nephropathy. Ideally, the blood glucose levels should be between 90-130 mg/dL(5.0-7.2 mmol/L) and hemoglobin A1c below 7%.
  • If the GFR progressively decreases inspite of tight glycemic control, the use and dose of oral hypoglycemics have to be reevaluated.
  • In presence of renal compromise, chlorpropamide has an exaggerated hypoglycemic effect, metfromin can cause lactic acidosis and thiazolidinediones may aggravate volume overload states.
  • Renal degradation of administered insulin decreases with reduction in GFR and hence the need to reduce the dose for appropriate glucose control.

Protein restriction

  • Protein restricted diets have been believed to not only temporarily reduce symptoms associated with uremia, but also slow the rate of decline in renal function at an earlier stage by reducing protein mediated hyperfiltration. [3]
  • The National Kidney Foundation, recommends patients with CKD to maintain a daily protein intake of 0.60 to 0.75 g/kg of body weight.

Proteinuria treatment with medications

Determining whether an anti-hypertensive medication reduces progression of kidney disease independently of the medication's lowering of blood pressure is difficult as demonstrated by the HOPE trial that originally reported of the benefit of ramipril on cardiovascular[8] and maybe renal[9] outcomes independently of blood pressure lowering, but later this was found to be due to the ramipril being taking at night and the blood pressure being measured 12 to 18 hours later[10].


Clinical practice guidelines by the Kidney Disease Improving Global Outcomes (KDIGO)[11] in the United States and National Institute for Health and Care Excellence (NICE)[12] in the United Kingdom guide management.

Meta-analyses summarize the evidence for erythropoiesis-stimulating agents affecting clinical[13] and quality-of-life[14][15] outcomes.

Based on the Federal Drug Administration erythropoietin EPO may be started when hemoglobin is < 10 g/dl, and its dose may be adjusted to maintain a target hemoglobin range of 10-12 g/dl. However, the National Kidney Foundation recommend maintaining a target hemoglobin range of 11-12 g/dl.

Many erythropoiesis-stimulating agents are available with no preparation having a clear advantage.[16]

Hypoxia-Inducible Factor-Prolyl Hydroxylase inhibitors show promise in preliminary studies.[17]

Electrolyte abnormalities

  • In chronic kidney disease vitamin D deficiency develops resulting in both hypocalcemia, and hypophosphatemia. Additionally, phosphorus excretion is effected. Thus, hypocalcemia is associated with hyperphosphatemia. In response to hypocalcemia, intact-PTH levels become elevated.
  • In stage 3 or 4 CKD, if intact-PTH is above goal, and calcium and phosphate levels are normal, vitamin D levels should be checked.
  • The therapy should be guided based on 25OH Vitamin D levels
    • If 25OH Vitamin D levels are >30 ng/ml and PTH intact is normal then no therapy is needed.
    • If 25OH Vitamin D levels are >30 ng/ml and PTH intact is above normal goal then daily therapy with an active vitamin D formulation, such as calcitriol is needed.
    • If 25OH Vitamin D levels are between 20-29 ng/ml, therapy with ergocalciferol or cholecaciferol 800-1000 IU daily should be initiated.
    • If 25OH Vitamin D levels are less than 20 ng/ml, therapy with ergocalciferol or cholecaciferol 50,000 IU weekly for 6-8 weeks followed by 800-1000 IU daily should be initiated.

Phosphorus management in CKD

Once the diagnosis of CKD is made check phosphorus levels and based on the levels following approach can be used:

Low phosphorus

  • Consider primary hyperparathyroidism.
  • Consider secondary hyperparathyroidism due to vitamin D deficiency.
  • Consider familial hypocalcuric hypercalcemia.

Normal phosphorus

  • Continue to follow

High phosphorus

  • Restrict dietary phosphorus
  • Initiate phosphate binder based on calcium level:
    • Low calcium - Use calcium based binder, calcium carbonate or calcium acetate
    • High calcium- Use non-calcium based phosphate binder, Sevelamer carbonate and lanthanum carbonate

Drug dose adjustments

Kidney Transplant

  • Offers the best potential for complete rehabilitation

Contraindicated medications

Severe or progressive kidney disease is considered a relative contraindication to the use of the following medications:

Severe Renal failure (creatinine clearance (CrCl) < 30ml/min) is considered an absolute contraindication to the use of the following medications:

Advanced renal impairment is considered an absolute contraindication to the use of the following medications:

Renal impairment (e.g., serum creatinine ≥1.5 mg/dL for men, ≥1.4 mg/dL for women, or abnormal creatinine clearance) is considered an absolute contraindication to the use of the following medications:

Hyperkalemia in chronic renal failure is considered a relative contraindication to the use of the following medications:

Patient education

Multidisciplinary approach

  • Explain likelihood and timing of initiation of renal replacement therapy and other options available
  • Discuss home based dialysis therapy
    • Less expensive
    • Improved quality of life
  • Counsel family members about home dialysis helper
  • Explore options to look for potential biologically related kidney donor

Contraindicated medications

Renal disease or renal dysfunction (e.g., as suggested by serum creatinine levels ≥1.5 mg/dL [males], ≥1.4 mg/dL [females], or abnormal creatinine clearance) is considered an absolute contraindication to the use of the following medications:

Marked renal dysfunction is considered an absolute contraindication to the use of the following medications:

End State Renal Disease is considered an absolute contraindication to the use of the following medications:

ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death - End-Stage Renal Failure (DO NOT EDIT) [18]

Class I
"1. The acute management of ventricular arrhythmias in end-stage renal failure should immediately address hemodynamic status and electrolyte (potassium, magnesium, and calcium) imbalance. (Level of Evidence: C). "
"2. Life-threatening ventricular arrhythmias, especially in patients awaiting renal transplantation, should be treated conventionally, including the use of ICD and pacemaker implantation as required, in patients who are receiving chronic optimal medical therapy, and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: C). "


  1. Ruggenenti P, Perna A, Gherardi G, Gaspari F, Benini R, Remuzzi G. Renal function and requirement for dialysis in chronic nephropathy patients on long-term ramipril: REIN follow-up trial. Gruppo Italiano di Studi Epidemiologici in Nefrologia (GISEN). Ramipril Efficacy in Nephropathy. Lancet. 1998 Oct 17;352(9136):1252-6. PMID 9788454.
  2. Ruggenenti P, Perna A, Gherardi G, Garini G, Zoccali C, Salvadori M, Scolari F, Schena FP, Remuzzi G. Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria. Lancet. 1999 Jul 31;354(9176):359-64. PMID 10437863.
  3. Aparicio M, Bellizzi V, Chauveau P; et al. (2012). "Protein-restricted diets plus keto/amino acids--a valid therapeutic approach for chronic kidney disease patients". Journal of Renal Nutrition : the Official Journal of the Council on Renal Nutrition of the National Kidney Foundation. 22 (2 Suppl): S1–21. doi:10.1053/j.jrn.2011.09.005. PMID 22365371. Unknown parameter |month= ignored (help)
  4. Chrysostomou A, Becker G (2001). "Spironolactone in addition to ACE inhibition to reduce proteinuria in patients with chronic renal disease". N Engl J Med. 345 (12): 925–6. doi:10.1056/NEJM200109203451215. PMID 11565535.
  5. Bakris GL, Agarwal R, Anker SD, Pitt B, Ruilope LM, Rossing P; et al. (2020). "Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes". N Engl J Med. 383 (23): 2219–2229. doi:10.1056/NEJMoa2025845. PMID 33264825 Check |pmid= value (help).
  6. EMPA-KIDNEY Collaborative Group. Herrington WG, Staplin N, Wanner C, Green JB, Hauske SJ; et al. (2022). "Empagliflozin in Patients with Chronic Kidney Disease". N Engl J Med. doi:10.1056/NEJMoa2204233. PMID 36331190 Check |pmid= value (help).
  7. Gerstein HC, Colhoun HM, Dagenais GR, Diaz R, Lakshmanan M, Pais P; et al. (2019). "Dulaglutide and renal outcomes in type 2 diabetes: an exploratory analysis of the REWIND randomised, placebo-controlled trial". Lancet. 394 (10193): 131–138. doi:10.1016/S0140-6736(19)31150-X. PMID 31189509.
  8. "Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of the HOPE study and MICRO-HOPE substudy. Heart Outcomes Prevention Evaluation Study Investigators". Lancet. 355 (9200): 253–9. 2000. PMID 10675071.
  9. Mann JF, Gerstein HC, Yi QL, Lonn EM, Hoogwerf BJ, Rashkow A; et al. (2003). "Development of renal disease in people at high cardiovascular risk: results of the HOPE randomized study". J Am Soc Nephrol. 14 (3): 641–7. doi:10.1097/01.asn.0000051594.21922.99. PMID 12595499.
  10. Taylor R (2003). "Conundrum of the HOPE study: time of taking ramipril may account for lack of relation between blood pressure and outcome". BMJ. 327 (7416): 681–2, author reply 682. doi:10.1136/bmj.327.7416.681-c. PMC 196432. PMID 14509993.
  11. "Chapter 1: Diagnosis and evaluation of anemia in CKD". Kidney Int Suppl (2011). 2 (4): 288–291. 2012. doi:10.1038/kisup.2012.33. PMC 4089684. PMID 25018948.
  12. Padhi S, Glen J, Pordes BA, Thomas ME, Guideline Development Group (2015). "Management of anaemia in chronic kidney disease: summary of updated NICE guidance". BMJ. 350: h2258. doi:10.1136/bmj.h2258. PMID 26044132.
  13. Palmer SC, Navaneethan SD, Craig JC, Johnson DW, Tonelli M, Garg AX; et al. (2010). "Meta-analysis: erythropoiesis-stimulating agents in patients with chronic kidney disease". Ann Intern Med. 153 (1): 23–33. doi:10.7326/0003-4819-153-1-201007060-00252. PMID 20439566. Review in: Ann Intern Med. 2010 Nov 16;153(10):JC5-3
  14. 14.0 14.1 Collister D, Komenda P, Hiebert B, Gunasekara R, Xu Y, Eng F; et al. (2016). "The Effect of Erythropoietin-Stimulating Agents on Health-Related Quality of Life in Anemia of Chronic Kidney Disease: A Systematic Review and Meta-analysis". Ann Intern Med. 164 (7): 472–8. doi:10.7326/M15-1839. PMID 26881842.
  15. 15.0 15.1 Cody JD, Hodson EM (2016). "Recombinant human erythropoietin versus placebo or no treatment for the anaemia of chronic kidney disease in people not requiring dialysis". Cochrane Database Syst Rev. 1: CD003266. doi:10.1002/14651858.CD003266.pub3. PMID 26790135.
  16. Palmer SC, Saglimbene V, Mavridis D, Salanti G, Craig JC, Tonelli M; et al. (2014). "Erythropoiesis-stimulating agents for anaemia in adults with chronic kidney disease: a network meta-analysis". Cochrane Database Syst Rev. 12: CD010590. doi:10.1002/14651858.CD010590.pub2. PMID 25486075.
  17. Brigandi RA, Johnson B, Oei C, Westerman M, Olbina G, de Zoysa J; et al. (2016). "A Novel Hypoxia-Inducible Factor-Prolyl Hydroxylase Inhibitor (GSK1278863) for Anemia in CKD: A 28-Day, Phase 2A Randomized Trial". Am J Kidney Dis. doi:10.1053/j.ajkd.2015.11.021. PMID 26827289.
  18. Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M; et al. (2006). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation. 114 (10): e385–484. doi:10.1161/CIRCULATIONAHA.106.178233. PMID 16935995.

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