Chronic Kidney Disease

Stages (1)

Stage I: GFR ≥ 90 mL/min

Stage II: GFR 60-89 mL/min

Stage IIIa: GFR 45-59 mL/min

Stage IIIb: GFR 30-44 mL/min

Stage IV: GFR 15-29 mL/min

Stage V: GFR <15 mL/min

Common Causes

  • Diabetes mellitus
  • Hypertension

Rarer Causes

  • Inherited Disorders
    • Polycystic Kidney Disease
    • Tubulointerstitial Disease
  • Decreased Renal Mass
    • Renal Agenesis
    • Nephrectomy
  • Severe or Recurrent Acute Disease States
    • Severe/prolonged AKI
    • Recurrent/Complicated UTI
  • Nephrotic Syndrome
  • Nephritic Syndrome
  • Chronic Disease States
    • Heart Failure
    • Cirrhosis
    • Renovascular Disease
  • Cancer
    • Multiple Myeloma
    • Renal Cell Carcinoma
  • Medications/Toxins
    • Chemotherapy (cisplatin (2), ifosfamide (3) are big culprits)
    • NSAIDs
    • Lithium
    • Lead exposure


  • Blood pressure and diabetes control
  • Treat underlying condition and remove offending agents
  • Slow the progression of proteinuria
    • ACE-Inhibitors
    • Angiotensin-Receptor Blockers
    • SGLT-2 Inhibitors (generally only in patients with concomitant diabetes, but more recently have been shown to be efficacious in patients without diabetes as well (4))
  • Treat complications as below


  • Acidemia
    • From retained anions and inability to excrete acid as renal function deteriorates
    • KDIGO recommends bicarbonate therapy if serum bicarbonate is chronically <22, which has been shown to slow the progression of renal disease
  • Anemia
    • From decreased amount of EPO production (see Anemia)
    • First, replete iron stores if deficient, then can supplement with EPO if anemia persists
  • Volume overload and hypertension
    • Patients with CKD and hypertension generally require a diuretic for blood pressure and volume control
  • Hyponatremia, hyperkalemia
    • Loop diuretics may serve as treatment
  • Hypocalcemia
    • As a result of decreased hydroxylation of 25-OH-Vitamin D into its active form (1,25-OH-Vitamin D) by renally-located enzyme 1-α-hydroxylase
    • Treatment: supplementation with cholecalciferol (Vitamin D3), as well as calcium supplementation to prevent secondary hyperparathyroidism as below. Though this vitamin still needs to be activated by 1-α-hydroxylase, it has been shown to have benefit in patients with CKD, who tend to have low 25-OH-Vitamin D levels (5)
  • Secondary Hyperparathyroidism (6)
    • Triggers
      • Hypocalcemia
      • Low Vitamin D levels
      • Hyperphosphatemia (from reduced GFR in CKD leading to increased phosphate reabsorption)
    • Pathophysiology
      • The above triggers cause an appropriately-increased PTH secretion, which in turn leads to increased bone turnover
    • Treatment (7)
      • Low phosphate diet
      • Phosphate binders (sevelamer)
      • Vitamin D
      • Calcimimetic agents (cinacalcet)
        • Activate CaSR -> decrease PTH production
  • Tertiary Hyperparathyroidism (8)
    • Progression of secondary hyperparathyroidism to the point of autonomous proliferation of the parathyroid gland so that excessive PTH secretion occurs regardless of calcium or vitamin D levels
    • Will typically see elevated calcium levels, decreased phosphate levels
    • Treatment: Parathyroidectomy
  • Dyslipidemia
    • Elevated triglycerides and low HDL
    • Pathophysiology involves complex biochemical pathways including decreased catabolism of triglyceride-rich lipoproteins, decreased apolipoprotein availability for HDL synthesis, and impairment of lecithin-cholesterol acyltransferase (the enzyme responsible for converting cholesterol into a cholesteryl ester that can be packaged into HDL) (9)
  • Uremia
    • Platelet dysfunction
    • Pericarditis
    • Encephalopathy


  1. Estimated glomerular filtration rate (egfr). (2020, September 14). Retrieved March 10, 2021, from
  2. Shi M;McMillan KL;Wu J;Gillings N;Flores B;Moe OW;Hu MC;. (n.d.). Cisplatin nephrotoxicity as a model of chronic kidney disease. Retrieved March 11, 2021, from
  3. KD;, A. (n.d.). Chronic Ifosfamide TOXICITY: Kidney pathology And pathophysiology. Retrieved March 11, 2021, from
  4. Heerspink, H., Al., E., For the DAPA-CKD Trial Committees and Investigators*, & Author AffiliationsFrom the Department Clinical Pharmacy and Pharmacology. (2021, January 28). Dapagliflozin in patients with chronic KIDNEY DISEASE: NEJM. Retrieved March 11, 2021, from
  5. Jean, G., Souberbielle, J., & Chazot, C. (2017, March 25). Vitamin d in chronic kidney disease and dialysis patients. Retrieved March 11, 2021, from
  6. Muppidi, V. (2021, January 06). Secondary hyperparathyroidism. Retrieved March 11, 2021, from
  7. Cozzolino, M., Galassi, A., Conte, F., Mangano, M., Lullo, L., & Bellasi, A. (2017, June 01). [Full TEXT] treatment of secondary HYPERPARATHYROIDISM: The clinical utility Of et: TCRM. Retrieved March 11, 2021, from
  8. Electron Kebebew, M. (2004, September 01). Tertiary hyperparathyroidism. Retrieved March 11, 2021, from
  9. Mikolasevic, I., Žutelija, M., Mavrinac, V., & Orlic, L. (2017, February 7). Dyslipidemia in patients with chronic kidney DISEASE: Etiology and management. Retrieved March 11, 2021, from

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