- CRF = abnormally low GFR for >3/12
- Causes: glomerulonephritis (30%), interstitial nephritis and reflux nephropathy (20%), polycystic kidneys (10%), DM (10%), renovascular disease/HTN (10%)obstructive uropathy and unknown causes (20%).
- Incidence of CRF suitable for renal replacement therapy 65-100/million/year
Functions of kidneys and effects of failure:
- Failure to regulate salt and water excretion = peripheral and pulmonary oedema. Inability to concentrate urine = nocturia
- HTN is severe enough = encephalopathy. Premature CVD accounts for much of mortality due to CRF. All linked to dyslipidaemia, HTN, chronic anaemia, abnormalities of calcium metabolism, RAA-system.
- Accumulation of nitrogenous waste = encephalopathy, hic-cough, pericarditis, N&V, pruritus, malaise, impotence, menstrual irregularities, neuropathy. Uraemia = anorexia, disturbances in protein metabolism, malnutrition, muscle wasting/weakness and inactivity
- Metabolic acidosis
- Anaemia = due to EPO deficiency, or reduced RBC lifespan, or GI bleeding. Mild anaemia in polycystic kidney disease, and severe in interstitial nephritides
- Renal bone disease – relates to osteomalacia (failure of renal hydroxylation of vit D), secondary hyperparathyroidism driven by chronic hypocalaemia (caused by high phosphate and low vit D) and nutritional osteoporosis. Aluminium bone toxicity may complicate haemodialysis.
- Increased bleeding tendency – due to depressed plt and vWF activity
- Infection – cellular and humoral immunity are impaired
- Hx of frequent UTIs (=reflux nephropathy)!
- FH of APKD = think APKD!
- Haematuria found in previous examinations – consider chronic GN
- If anaemic or kidneys are small – likelihood is that the problem is chronic. Always look for acute causes – as if diagnosed early maybe reversible.
- Drugs: EPO and iron (correct anaemia), 1-alpha-Vit D (increase Ca2), phosphate binders (reduce phosphate), anti-hypertensives (lower BP), loop diuretics (reduce sodium and water)
- Renal tract USS (exclude obstruction and document kidneys size).
- If the cause is unclear and kidneys are normal size – take a biopsy.
- Rule of SLE, vasculitis, myeloma, and proteinuria
- Severity of renal failure determined by creatinine, urea, and creatinine clearance.
- Once failure begins – there is a slowly progressive failure over several years (possibly due to hyperfiltration through remaining glomeruli). Slow this by aggressive anti-HTN tx (reduce pressure on remaining glomeruli).
- End-stage renal failure (ESRF) = term used when pts would not survive without renal replacement therapy (=haemodialysis/peritoneal dialysis/transplantation).
- It is important to create good dialysis access before uraemic symptoms arise
- Before dialysis – correct calcium (tx = 1-alpha-hydroxycholecalciferol) and phosphate imbalances (phosphate binders), anaemia (EPO), acidosis (sodium bicarbonate), HTN (A,C,A&C…), sodium and water retention (diuretics)
Indications for dialysis:
- Uraemic symptoms and creatinine >500micro mol/L
- Life-threatening complications = hyperkalaemia, acidosis, fluid overload, uraemic pericarditis/encephalopathy.
- o Gain vascular access via arteriovenous fistula (needs 8/52 to ‘mature’ before use), or by using double lumen jugular/subclavian/femoral lines
- o The diffusion of solutes and water occurs across a semi-permeable membrane, which separates blood and dialysate flow in opposite directions.
- o Can cause cardiovascular instability – due to concurrent CVD and drugs use for its Tx, as well as major fluid shifts that occur during dialysis
- o Dialysis membranes activate the clotting cascades so heparin is used to reduce this.
- o Most membranes do not allow removal of beta-2-microglobulin which accumulates causing carpal tunnel and arthropathy
- o Over-rapid removal of toxic metabolites causes profound illness = ‘dialysis disequilibrium’. Prevented by small regular dialysis txs.
- o Pros: no immunosuppression needed, suitable for all patient sizes
- o Cons: risks of CVD, costs £20,000/year, inconvenient (takes 3 x 4hours / week), fluid restrictions apply, need a vascular access point)
- Continuous ambulatory peritoneal dialysis:
- o Instil several litres of isotonic/hypertonic glucose solution QDS for several hours into the peritoneal cavity via a permanent catheter.
- o The peritoneal lining acts as a dialysis membrane.
- o After several hours the fluid now containing solutes and waste products is drained out.
- o Excess body fluids are removed by using hypertonic solutions.
- o Pros: cheap and does not require immunosuppression
- o Cons: risks of CVD, inconvenient carrying around litres of fluid, have to restrict fluid intake, not suitable for larger patients.