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238 Chapter 6: Genitourinary system
2 Excretion of waste products, drugs and toxins is Macroscopy/microscopy
reduced leading to complications of toxicity. The kidneys are usually small and shrivelled, with
3 The hormone functions of the kidney are also affected: scarring of glomeruli, interstitial fibrosis and tubular at-
reduction of vitamin D activation causes hypocal- rophy.
caemia and hyperparathyroidism; reduced erythro-
poietin production causes anaemia.
As renal function declines to about 10–20% of normal, Investigations
i.e. a GFR of ∼15 mL/min, symptoms develop. Acute The aim of investigations is to make a diagnosis of the
renal failure (ARF) may also lead to these symptoms, cause, and in addition, to consider if there is any acute
although they are more commonly seen in CRF. This condition precipitating the renal failure, e.g. prerenal
is called uraemia – which literally means ‘urine in the failure, sepsis, obstruction or a nephrotoxin. Any pre-
blood’. The onset of uraemia is insidious, but by the time vious historical urea and creatinine measurements are
serum urea is >40 mmol/L, creatinine >1000 µmol/L, very useful.
most patients have symptoms. No single toxin has been The investigations for ARF on CRF or undiagnosed
identified, and in fact urea itself is not thought to be CRF are similar to those for ARF (see page 235), in-
very toxic, but it acts as a convenient marker for other cluding the blood tests, imaging and possibly renal
products. biopsy.
Chronic renal failure is now classified as stages 1–5
of chronic kidney disease, according to GFR and other
Clinical features features (see Table 6.6).
The onset of symptoms is variable. Early symptoms In the routine follow-up of CRF, the usual investiga-
are mostly due to anaemia (malaise, fatigue and short- tions include the following:
ness of breath on exertion). Late symptoms include FBC to look for anaemia.
pruritis, anorexia, nausea and vomiting – very late U&E to assess progress of the renal failure, ensure Na +
+
symptoms are pericarditis, encephalopathy (confusion, and K are normal.
coma, seizures) and tachypnoea due to metabolic acid- Bicarbonate to look for acidosis.
osis. Calcium, phosphate, ALP, PTH (X-ray hands to assess
There are few signs of ESRF, although there may for renal osteodystrophy).
be signs of the underlying cause such as diabetic CRP (ESR is normally raised in CRF, but a raised CRP
retinopathy, renal or femoral bruits, an enlarged prostate suggests infection).
or polycystic kidneys. It is important to assess the Hyperlipidaemia should be looked for.
fluid status by looking at the jugular venous pressure, Urinalysis is performed to look for proteinuria and
skin turgor, lying and standing blood pressure, and haematuria (if new or increasing these may need fur-
for evidence of pulmonary or peripheral oedema (see ther investigation) and urinary tract infections.
Fig. 6.6). Underlying causes may need to be monitored, e.g.
HbA 1 C for diabetes mellitus and urate for gout.
Complications
Table 6.6 Staging of chronic kidney disease (CKD)
CRF patients are much more prone to ARF (acute-
on-chronic renal failure), for example due to drugs, Stage 1 CKD Kidney damage but normal GFR (>90
radiographic contrast and dehydration. Patients with mL/min)
Stage 2 CKD Mild kidney damage (GFR 60–89
CRF are affected by accelerated atherosclerosis which
mL/min)
occurs due to long-term hypertension, hyperlipidaemia, Stage 3 CKD Moderate kidney damage (GFR 30–59
disorderedcalciumandphosphatemetabolism(calcified mL/min)
vessels) and uraemia. They also develop left ventricular Stage 4 CKD Severe kidney damage (GFR 15–29
hypertrophy due to hypertension. Cardiovascular mor- mL/min)
Stage 5 CKD Kidney failure (GFR <15 mL/min or
bidity and mortality are much higher than in patients
ESRF on renal replacement therapy)
with normal renal function.