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Chapter 6: Disorders of the kidney 237

sympathetic activity and the release of vasoconstrictive Table 6.5 Causes of chronic renal failure
substances. The glomerular filtration rate (GFR) falls
Uncertain 19%
in response to hypoperfusion, and ischaemia causes the Diabetes mellitus 17%
tubules to lose function. Glomerulonephritis 12%
Toxinsmayhaveavarietyofmechanismssuchascaus- Pyelonephritis/reflux nephropathy 10%
ing vasoconstriction, a direct toxic effect on tubular cells Renovascular disease 7%
Hypertension 6%
causing their dysfunction, and they may also cause the
Adult polycystic kidney disease 6%
death of tubular epithelial cells which block the tubules. Other (inc. not sent) 23%
The glomeruli (which are well perfused) may continue
to filter urine in large volumes, and if the tubules are not
reabsorbing the filtrate, urine output may be maintained Chronic renal failure
(non-oliguric renal failure) or even increased (polyuric
Definition
renal failure).
Chronic renal failure (CRF) is a loss of renal function oc-
Ischaemia or toxins can cause tubular epithelial cells
curring over months to years because of the destruction
to die and slough away from the basement membrane,
of nephrons. End-stage renal failure (ESRF) is loss of
blockingthetubules.Blockageoftherenaltubulescauses
renal function requiring any form of chronic renal re-
asecondary reduction in glomerular blood flow.
placement therapy, i.e. long-term dialysis or transplan-
If the basement membrane is intact, tubular epithe-
breaktation.
lium regrows within 10–20 days, restoring function to
the nephrons. Dead material is phagocytosed. The ep- Incidence
ithelial cells take time to differentiate and develop their The exact number of people with chronic renal failure is
concentrating function. difficult to estimate, as many are undetected. The num-
ber who progress to end-stage renal failure and com-
mence renal replacement therapy is ∼100 per million
Clinical features
ATNpresents as with acute renal failure. It typically population per year in the U.K.
passes through three phases:
Aetiology
Oliguricphase(reducedGFR):Acuterenalfailurewith

The main causes in England and Wales (2002) are listed
complications of hyperkalaemia, metabolic acidosis
in Table 6.5. Certain systemic diseases commonly cause
and fluid overload (pulmonary oedema). This phase
renal disease such as amyloid, myeloma, systemic lupus
may last many weeks, depending on the initial severity
erythematosus and gout.
of insult.
Ina significant proportion of patients no underlying
Polyuric phase: This is during early recovery, patients

cause is found. These patients are often labelled as ESRF
may pass 5 L or more of urine a day and are at risk of
secondary to hypertension, but this may be a result of
developing secondary problems with water and elec-
the renal failure rather than the cause.
trolyte (Na ,K ,Ca ++ )depletion.Initially uraemia
+
+
may persist, but this usually gradually improves.
Pathophysiology
Recovery to baseline renal function, or with some

Progressive destruction of nephrons leads to gradual re-
residual deficit.
ductioninrenalfunction,withlossofthethreefunctions
of the kidney:
Management 1 Electrolyte and water homeostatic disturbance may
The management is similar to that of acute renal failure. cause fluid overload, hypertension, hyperkalaemia
and metabolic acidosis as well as rises in serum urea
and creatinine. Initially there may be a phase of large
Prognosis volumes of dilute urine production due to reduction
In acute tubular necrosis the mortality is high but if in tubular reabsorption. As the glomerular filtration
the patient survives the prognosis for renal recovery is rate (GFR) falls further urine volumes fall to less than
good. normal.