CKD

• Chronic kidney disease is defined as an abnormal kidney function or structure present for greater than three months, with subsequent implications for health
• Pathophysiology:

  • End stage for any cause of severe and/or long standing kidney injury
  • Damage to the kidneys reduces the number of functioning nephrons - leads to hyperfiltration at the glomeruli and increases glomerular permeability - development of proteinuria
  • Activation of the RAAS causes an increase in blood pressure which worsens the hyperfiltration at the glomerular level
  • Increase in capillary pressure within the glomerulus and inflammatory mediators cause chronic inflammation
• CKD is classified by the eGFR and amount of proteinuria

  • Albuminuria >30 mg/mmol = severely increased
  • G1 = eGFR >90 (normal) but with albuminuria
  • G2 = eGFR 60-89
  • G3a = eGFR 45-59
  • G3b = eGFR 30-44
  • G4 = eGFR 15-29
  • G5 = eGFR <15 - established renal failure
• Causes of CKD:

  • The most common causes in adults are diabetes and vascular disease
  • Glomerular disease
  • Nephrotoxic drugs - aminoglycosides, ciclosporin, PPIs, NSAIDs
  • Obstructive uropathy
  • Multisystem diseases with renal involvement - SLE, vasculitis, HIV
  • Polycystic kidney disease
  • Prostate pathology
• Risk factors for CKD:

  • Age over 50
  • History of AKI
  • History of childhood kidney disease
  • Family history of CKD stage 5
  • Diabetes
  • Cardiovascular disease
  • Gout - risk factor for renal stones
  • Solitary functioning kidney
  • Smoking
• CKD is primarily asymptomatic, and symptoms usually only start developing at an advanced stage (4-5)

  CKD is usually detected through the presence of hypertension, haematuria, proteinuria, or a reduction in GFR with increased serum creatinine
• Symptoms of advanced CKD:

  • General symptoms - fatigue, nausea and vomiting, cramps, insomnia, restless legs, bone pain and pruritus
  • Abnormal urine output - polyurea, oliguria and nocturia
  • Fluid overload - may present as dyspnoea and orthopnoea
  • Sexual dysfunction
  • Severe uraemia may also cause hiccups, pericarditis, coma and seizures
• Bedside investigations for CKD:

  • Blood pressure - usually raised
  • Urinalysis - haematuria and/or proteinuria
  • Capillary blood glucose - to detect undiagnosed diabetes or assess control of diabetes
  • ECG
• Laboratory investigations for CKD:

  • FBC - normochromic, normocytic anaemia due to erythropoietin deficiency
  • U&Es - elevated creatinine and reduced eGFR, raised potassium and low bicarbonate
  • Serum albumin - hypoalbuminaemia
  • Urinary albumin - albumin to creatinine ratio increased
  • Serum phosphate - elevated
  • Serum PTH - rises as GFR falls due to secondary hyperparathyroidism
  • Cholesterol - commonly raised
• Patients need screening for Hepatitis B and C, and HIV before starting dialysis
• Imaging for CKD:

  • Plain abdominal xray - may reveal renal stones
  • Renal USS - structural abnormalities. Advanced CKD often leads to small echogenic kidneys
  • CT or MRI
• Normal size of kidneys:

  • 10-14cm in males
  • 9-13cm in females
• A diagnosis of CKD requires evidence of kidney damage and/or a persistent reduction in renal function.

  CKD stages 3 – 5 can be diagnosed based on GFR alone (<60 mL/min/1.73m2).
• For diagnosis of CKD stages 1-2, additional evidence of renal disease is required:

  • Proteinuria
  • Urine sediment abnormalities
  • Electrolyte abnormalities
  • Histological abnormalities
• General management of CKD:

  • Life style modification
  • Good glycaemic control
  • Control of hypertension - ACE inhibitor first line, SGLT-2 can be added
  • Influenza and pneumococcus immunisations
  • Avoid nephrotoxic medication
  • Diet - high protein, low sodium and phosphate
  • Vitamin D supplements
  • Erythropoietin stimulating agent for anaemia
• Renal replacement therapy is an important aspect of the treatment of end stage CKD

  Includes haemodialysis, peritoneal dialysis and kidney transplantation
• When patients receive a kidney transplant, their native kidneys are normally left in situ (unless large polycystic kidneys). The donor kidney is placed in the iliac fossa
• Patients with CKD are usually profoundly anaemic. This is due to the kidneys producing insufficient erythropoietin. Patients usually do not receive transfusions as this can cause sensitisation prior to kidney transplantation
• Cardiovascular disease is a common complication of CKD:

  Activation of the RAAS causes water and sodium overload. This further worsens the hypertension.

  There is also accelerated atherosclerosis
• Patients with CKD can develop peripheral neuropathy due to uraemia
• CKD also decreases the metabolic rate of the brain, which can lead to cognitive impairment
• Renal bone disease in CKD:

  • CKD causes low vitamin D
  • Decreased vitamin D causes hypocalcaemia
  • Causes excess PTH - secondary hyperparathyroidism
  • Slow bone growth and fractures
  • Bone pain
• Typical clinical findings in CKD may include:3,6

  • Uraemic fetor: ammonia-like smell of the breath
  • Pallor: due to anaemia
  • Cachexia
  • Cognitive impairment: specifically affecting language, orientation and attention
  • Tachypnoea: may be due to fluid overload, anaemia
  • Hypertension
  • Volume disturbance: volume overload (e.g. peripheral oedema, pulmonary oedema, pleural effusions, ascites) or volume depletion
  • Peripheral neuropathy
  • Fundoscopy may reveal microvascular damage in patients with diabetes or hypertension
• There may be specific clinical findings depending on the underlying cause of CKD:

  • Bilateral masses upon palpation of flanks, suggestive of adult polycystic kidney disease. May be accompanied by hepatomegaly due to liver cysts.
  • Palpable bladder: may suggest obstructive uropathy, often accompanied by prostatic enlargement in men
• Patients should be assessed for cardiovascular risk factors (lipid profile, BMI, exercise, and alcohol and smoking consumption) and offered a statin and antiplatelet drug for the prevention of cardiovascular disease.
• Dietary phosphate restriction and phosphate binders (e.g. calcium acetate, sevelamer, lanthanum) to control hyperphosphataemia.
• Complications - acid base balance:

  • Metabolic acidosis
  • Due to the inability of the kidneys to excrete acid
  • Inability to secrete bicarbonate
  • Manged with oral bicarbonate supplements or dialysis
• Complications - electrolyte balance:

  • Hyperkalaemia
  • Kidneys inability to excrete potassium
  • Restriction of dietary potassium intake
  • Avoid hyperkalaemia promoting drugs e.g. ACE inhibitors
  • Oral potassium binders
  • Dialysis
• May be specific clinical findings depending on underlying cause:

  • Bilateral masses upon palpation of flanks - polycystic kidney disease
  • Palpable bladder - obstructive uropathy