Renal failure (chronic)
D E FI N I T ION
Chronic renal failure or chronic kidney disease (CKD) is defined as either
kidney damage or GFR <60 mL/min/1.73m2 for 3 months. Kidney damage is defined as
pathologic abnormalities or markers of damage, including abnormalities in blood or urine
tests or imaging studies.
Stage GFR (mL/min/1.73m2)
1 90
2 60–89
3 30–59
4 15–29
5 <15
AE T IOLOGY
Diabetes mellitus and hypertension are the two most common causes.
Vascular disease: Hypertension, renal artery atheroma, vasculitis.
Glomerular disease: Glomerulonephritis, diabetes, amyloid, SLE.
Tubulointerstitial disease: Pyelonephritis/interstitial nephritis, nephrocalcinosis, tuberculosis.
Obstruction and others: Myeloma, HIV nephropathy, scleroderma, gout, renal tumour,
inborn errors of metabolism (e.g. Fabry’s disease).
Congenital/inherited: Polycystic kidney disease, Alport’s syndrome, congenital hypoplasia.
E P IDEMIOLOGY
Incidence of end-stage CRF in England >110 per million population per
year. Higher incidence in Asian immigrants than native British population.
H ISTORY
Anorexia, nausea, malaise, pruritus. Later: diarrhoea, drowsiness, convulsions,
coma.
Symptoms of the cause and other complications.
EXAMINA T I ON
Systemic: Kussmaul’s breathing (acidosis), signs of anaemia, oedema,
pigmentation, scratch marks.
Hands: Leuconychia, brown line at distal end of nail.
There may be an arteriovenous fistula (buzzing lump in wrist or forearm).
Signs of complications (e.g. neuropathy, renal bone disease).
INVE S T I G A T IONS
Blood: FBC (# Hb: normochromic, normocytic), U&E (# urea and
creatinine), eGFR (can be derived from creatinine and age using the MDRD calculator),
#Ca2þ
, " phosphate, AlkPhos, PTH.
Investigate for suspected aetiology: e.g. ANCA, ANA, glucose.
24-h urine collection: Protein, creatinine clearance (which is a rough estimate of GFR).
Imaging: Signs of osteomalacia and hyperparathyroidism. CXR may show pericardial effusion
or pulmonary oedema.
Renal ultrasound: Measure size, exclude obstruction and visualize structure.
Renal biopsy: For changes specific to the underlying disease, contraindicated for small kidneys.
MANAGEMENT
Treat the underlying cause: Control diabetes
Manage complications of chronic kidney disease:
. Anaemia: Correct iron stores. Regular IV or SC erythropoietin (usually monthly).
. BP control: ACE inhibitors and Angiotensin-II antagonists (caution with renal artery stenosis).
. Hypocalcaemia: Maintain serum levels with 1-hydroxylated vitamin D analogues, e.g.
alfacalcidol. Consider bisphosphonates.
. Diet: High-energy intake, potassium intake restriction (in hyperkalaemia or acidosis,
oral NaHCO3 may be required), restriction of protein and phosphate intake (using
phosphate binders, e.g. calcium bicarbonate or aluminium hydroxide to # phosphate
absorption).
Renal failure (chronic) (continued)
. Drugs: Avoid nephrotoxic drugs (e.g. NSAIDs). Dose adjustments for drugs excreted from
kidneys.
. Oedema: Diuretics, e.g. furosemide (frusemide), metolazone.
Renal replacement therapy:
. Peritoneal dialysis (CAPD): Dialysate is introduced and exchanged through a ‘Tenkoff’
catheter, inserted via a subcutaneous tunnel into the peritoneum.
. Haemodialysis: Blood is removed via an arteriovenous fistula surgically constructed in the
wrist or forearm to provide high flow. Uraemic toxins are removed by diffusion across a
semipermeable membrane in an extracorporeal circuit (this may activate coagulation so
patients are heparinized).
. Renal transplantation: Requires long-term immunosuppressants to # rejection (e.g.
steroids, ciclosporin A, tacrolimus, azathioprine, daclizumab).
COMPL I C A T IONS
Haematological: Anaemia (# erythropoietin production, # marrow
activity, # RBC survival, # dietary Fe/folate, " blood loss: haemodialysis/sampling),
abnormal platelet activity (bruising, epistaxis).
CVS: Accelerated atherosclerosis, " BP, pericarditis.
Neuromuscular: Peripheral & autonomic neuropathy, myopathy.
Renal osteodystrophy: Osteoporosis, osteomalacia (# 1a-hydroxylation of vitamin D), secondary
or tertiary hyperparathyroidism, adynamic bone disease (# bone turnover and
fractures secondary to excessive suppression of the parathyroid gland with current
therapies), osteosclerosis.
Endocrine: Amenorrhoea, erectile impotence, infertility.
Peritoneal dialysis: Peritonitis (e.g. staphylococcus epidermidis).
Haemodialysis:
. Acute: Hypotension (excessive removal of extracellular fluid).
. Long-term:
* Atherosclerosis.
* Sepsis (secondary to peritonitis, Staph. aureus infection).
* Amyloidosis: Failure of removal of b2-microglobulin (component of HLA molecules) by
dialysis membranes ! periarticular deposition ! arthralgia (e.g. shoulder) and carpal
tunnel syndrome.
* Aluminum toxicity: Accumulation of aluminum from the dialysis fluid and phosphate
binders ! dementia, osteodystrophy, microcytic anaemia (rare).
Transplantation/immunosuppression: " BP, opportunistic infections (e.g. CMV), malignancies
(lymphomas and skin), recurrence of renal disease (e.g. Goodpasture’s syndrome), sideeffects
of drugs (e.g. steroids: features of iatrogenic Cushing’s syndrome; ciclosporin:
gum hyperplasia).
P ROGNOS I S
Depends on complications. Timely dialysis and transplantation " survival.
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