Complications of Chronic Renal Failure

Complications of Chronic Renal Failure

Uraemia

·         Symptom complex associated with severe, near end-stage renal failure (ie GFR < 20 mls/min)

·        Leads to:

o  Accumulation of uraemic toxins

o  Anaemia

o  Hyperparathyroidism

o  Metabolic acidosis

·        Common symptoms (NB some of these may be due to anaemia alone): 

o  CNS: Fatigue, weakness, malaise, ¯concentration, restless legs, insomnia

o  GI: anorexia, nausea, vomiting, gastritis 

o  Blood: anaemia, platelet dysfunction (® bleeding)

o  CVS: hypertension, oedema, pericarditis

o  Skin: pruritis, pigmentation

o  Endocrine: hyperlipidaemia, hypogonadism (® infertility and amenorrhoea), impotence

·        Investigations:

o  Serum creatinine and urea: markers of uraemia but also affected by malnutrition and muscle mass 

o   Creatinine clearance: overestimates GFR in severe renal failure as some Cr is secreted in the tubule

o  Albumin: marker of malnutrition and key prognostic factor

o  Ca, PO4 and PTH: markers of renal osteodystrophy

o  HCO₃: degree of metabolic acidosis

o  Anaemia due to ¯erythropoietin (but exclude other causes, eg ¯Fe or folate)

·        Management:

o  Protein restriction (but beware malnutrition)

o  Alkalis (eg HCO₃) to control acidosis

o  Aggressive blood pressure control

o  Fluid restriction if pulmonary oedema

o  K restriction and avoiding K increasing drugs 

o  Dialysis if these measures fail to control symptoms/signs.

Anaemia

·        Normocytic, normochromic

·        Universal in patients with end-stage renal failure (except that it‟s less common in polycystic disease) 

·        Secondary to erythropoietin deficiency, plus also ¯ RBC survival

·        Also ¯Fe and folate due to dialysis

·        Management:

o  Blood transfusion: effective but only temporary benefit. Complications: Fe overload, development of cytotoxic antibodies (® problems for future renal transplant)

·        Synthetic erythropoietin: Very effective, including ­well-being, exercise tolerance, ¯LV hypertrophy, etc. Most are Fe deficient, so need supplementation (maybe iv). Complications: worsening hypertension

Secondary Hyperparathyroidism 

·        Pathogenesis: 

o   ¯1,25 (OH)2D3 [calcitrol] from kidneys ® ¯Ca absorption and ­PTH

o   Renal failure ® ¯PO4 excretion ® ­serum PO4 ® ­PTH

o   ­PTH in most patients with GFR < 50 mls/min

·        Presentation:

o   Pruritis (?soft tissue deposition of calcium phosphate)

o   Bone pain due to calcium resorption

o   Restless legs

·        Management:

o   Early replacement of calcitrol (but watch for hypercalcaemia) 

o   Phosphate reduction: ¯dietary intake and calcium carbonate (binding agent in the gut ® ¯absorption) 

o   If these don‟t control the ­PTH without causing ­Ca, then parathyroidectomy (® hypocalcaemia and requirement for ongoing calcitrol)

Other complications

·        Hyperphosphataemia

·        Vascular disease

·        Chronic fluid overload ® LV hypertrophy and ­ BP