An 85-year-old woman is investigated by her general practitioner (GP) for increasing tiredness

which has developed over the past 6 months. She has lost her appetite and feels constantly
nauseated. She has lost about 8kg in weight over the past 6 months. For the last 4 weeks she has
also complained of generalized itching and cramps. She has been hypertensive for 20 years and
has been on antihypertensive medication for that time. She has had two cerebrovascular
accidents which have limited her mobility. She is an AfricanCaribbean, having emigrated to the
UK in the 1960s. She lives alone but uses a meals on wheels service and goes to a day hospital
twice a week. She has two daughters.

Examination Her conjunctivae are pale. Her pulse is 88/min regular, blood pressure
190/110mmHg; mild pitting oedema of her ankles is present. Otherwise, examination of her
cardiovascular and respiratory systems is normal. Neurological examination shows a left upper
motor neurone facial palsy with mild weakness and increased reflexes in the left arm and leg.
She is able to walk with a stick. Funduscopy shows arteriovenous nipping and increased
tortuosity of the arteries.

Questions

1. What is the diagnosis?

2. How would you investigate and manage this patient?

Answer:
This patient presents with the typical symptoms of end-stage renal failure, namely anorexia,
nausea, weight loss, fatigue, pruritus and cramps. The elevated urea and creatinine levels
confirm renal failure but do not distinguish between acute and chronic renal failure. Usually,
in the former, there is either evidence of a systemic illness or some other obvious
precipitating cause, e.g. use of nephrotoxic drugs/prolonged episode of hypotension, whereas
in the latter there is a prolonged history of general malaise. If the patient has had previous
blood tests measuring serum creatinine, these will be informative about the progression of
deterioration of renal function. In this patient, the anaemia and hyperparathyroidism (raised
alkaline phosphatase) are features indicating chronicity of the renal failure. The
normochromic, normocytic anaemia is predominantly due to erythropoietin deficiency (the
kidney is the major source of erythropoietin production). Hyperparathyroidism is a result of
elevated serum phosphate levels due to decreased renal clearance of phosphate and reduced
vitamin D levels (the kidney is the site of hydroxylation of 25-hydroxycholecalciferol to the
active form 1,25-dihydroxycholecalciferol). A hand X-ray showing the typical appearances
of hyperparathyroidism (erosion of the terminal phalanges and subperiosteal erosions of the
radial aspects of the middle phalanges), implying long-standing renal failure can be helpful in
distinguishing chronic and acute renal failure. Renal ultrasound is the essential investigation.
Ultrasound will accurately size the kidneys, and identify obvious causes for renal failure such
as polycystic kidney disease or obstruction causing bilateral hydronephrosis. Asymmetrically
sized kidneys suggest reflux nephropathy or renovascular disease. In this case, ultrasound
showed two small (8cm) echogenic kidneys consistent with long-standing renal failure. A
renal biopsy in this case is not appropriate as biopsies of small kidneys have a high incidence
of bleeding complications, and the sample obtained would show extensive glomerular and
tubulo-interstitial fibrosis and may not identify the original disease. The patients renal
failure may have been due to hypertension, or a primary glomerulonephritis such as IgA
nephropathy. AfricanCaribbeans are more prone to develop hypertensive renal failure than
other racial groups. Antihypertensive medications are needed to treat her blood pressure
adequately, oral phosphate binders and vitamin D preparations to control her secondary
hyperparathyroidism, and erythropoietin injections to treat her anaemia. The case raises the
dilemma of whether dialysis is appropriate in this patient. Hospital-based haemodialysis or
home-based peritoneal dialysis are the options available. Her age and comorbid illnesses
preclude renal transplantation. Conservative management without dialysis may be
appropriate in this case (Rees, P John, 2007).