Renal disease

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11 Renal disease

Questions

How do you calculate the plasma creatinine clearance value at the bedside, by body weight?

Can you tell me whether administering low doses of dopamine to increase renal blood flow is today considered obsolete?

Why does haemoglobinuria cause anuria?

I am confused over the use of a ‘high-protein diet’ in the management of nephrotic syndrome. You say it confers no advantage, but the Oxford Handbook of Clinical Medicine advocates its use and Davidson’s Principles and Practice of Medicine says it is even dangerous as it could lead to renal damage. Which one should I choose, assuming I see the question in an MCQ?

Is albumin infusion contraindicated in nephrotic syndrome? If not, then what are the indications?

Listed under the drug causes of nephrotic syndrome, it has been stated that high doses of captopril can induce an immune-complex-mediated membranous glomerulonephritis. If a patient with nephrotic syndrome has hypertension, is it detrimental to give captopril as a treatment for his hypertension? Could this exacerbate the patient’s nephrotic syndrome?

Please explain the pathophysiology of ascites in the nephrotic syndrome?

Does the nephritic syndrome cause hyperkalaemia? I don’t seem to be able to find a definitive answer in the textbooks that I have consulted.

You say that the investigation of first choice for urinary tract infections (UTIs) in males or children, or recurrent UTIs in females, is intravenous urography (IVU); in Oxford Handbook of Clinical Medicine it is ultrasound (US). Which is best?

1. Other than amoxicillin, what other orally administered drug is recommended for the treatment of a urinary tract infection (UTI) caused by enterococcus?

2. What is the recommended dosage for antibiotics in the prophylactic treatment of recurrent UTI in pregnancy? Is amoxicillin clavulanic acid safe to use during pregnancy?

What is the advantage of intermittent self-catheterization over an indwelling catheter? How is bladder training done while on an indwelling catheter?

Kindly tell me about the role of pulse wave velocity (PWV) in early diagnosis of arteriosclerosis. How is it useful in cardiac, diabetic and renal medicine?

You say that no convincing evidence was found that chronic hyperuricaemia causes nephropathy and nor can it be corrected by allopurinol. However, some patients we see have high serum uric acid and creatinine, which both come down with allopurinol. Please comment.

Can aspirin cause analgesic nephropathy? If yes, then how could we justify its use in primary prevention of coronary artery disease (CAD), even in high-risk patients? I have read that regular use of analgesics for 3 years could cause analgesic nephropathy.

What is the probability that a patient on a moderate daily dose of non-steroidal anti-inflammatory drugs (NSAIDs; ibuprofen 800mg once daily for tension headache) will develop analgesic nephropathy?

Do daily doses of paracetamol with the dosage range of 1g/day cause analgesic nephropathy. If so, after what length of time?

Allopurinol is used for the treatment of uric acid stones; it is also one of the aetiologies of renal calculi. Could you please explain its actual effect.

Why should we avoid angiotensin-converting enzyme (ACE) inhibitors as hypertensive therapy in the presence of renal artery stenoses? How can they lead to acute renal failure? What else can we prescribe for this patient to regulate the hypertension?

Is the use of angiotensin-converting enzyme (ACE) inhibitors contraindicated in cases of unilateral renal artery stenosis?

1. How effective is renal duplex in detecting renal artery stenosis?

2. Is magnetic resonance angiography superior to renal duplex in detecting renal artery stenosis?

How accurate is ultrasonography in detecting renal calculi?

Please explain the most effective way to manage a case of intrauterine fetal unilateral hydronephrosis in the 32nd week of pregnancy.

In renal failure, why does oedema first occur in the periorbital area and nowhere else?

How does sodium valproate decrease serum urea concentration and GI bleed increases it? Renal disease

1. What clinical information can be obtained by checking the blood urea nitrogen (BUN) level that cannot be obtained by checking the blood urea and serum creatinine alone?

2. What is the signifying difference between blood urea and BUN?

1. Does uraemia cause dysentery with blood and mucus mixed with the stools?

2. Is it correct to use the term ‘uraemic dysentery’?

3. Does uraemia cause finger clubbing?

What are the causes of a low serum creatinine?

Why does oliguria occur in the early stages of acute tubular necrosis (ATN)?

Is renal impairment induced by lithium therapy in bipolar affective disorders irreversible? How often does it occur?

Can you please explain why a patient with chronic renal failure (CRF) might present with either oliguria or polyuria?

What are uraemic frost conditions?

What is the role of terlipressin or novapressin in the management of hepatorenal syndrome?

What is the rationale of angiotensin-converting enzyme (ACE) inhibitors in chronic renal disease?

What procedure is recommended for post renal transplant if this is the second graft?

Do the cysts in autosomal-dominant polycystic kidney disease (PCKD) undergo malignant transformation and in what percentage?

In a 69-year-old patient with a 2-cm hard prostatic nodule on digital rectal examination, what is the more appropriate way to make a definitive diagnosis of prostate cancer: prostate biopsy or serum prostate-specific antigen (PSA)?

A 50-year-old patient complains from slight lower urological symptoms (mild difficulty in urination). By digital rectal examination a mass of (1) hypertrophy can be palpated. His family history contains cases of prostate cancer (in some relatives). What is the next investigation to do in this patient?

• Titration of serum prostate-specific antigen (PSA): Is it useful in such a patient? Why?

• Transrectal ultrasound (TRUS)?

• TRUS-guided needle biopsy?

What are the causes of urinary incontinence in the elderly?

For how long could urinary retention persist after major gastrointestinal tract surgery? Will cholinesterase inhibitors be of benefit in enhancing emptying of the bladder?

1. What are the possible causes of a large, white kidney?

2. What is the physiological significance of a giant cell?

What is the amount of 24-hour urinary albumin excretion above which a diabetic patient is said to have microalbuminuria?

How is forced diuresis induced in cases of prerenal failure?

The Cockcroft-Gault method is widely used:

The Modification of Diet in Renal Disease (MDRD) is another measure that uses serum creatinine level, sex and ethnicity to calculate estimated glomerular filtration rate (eGFR). It is calculated automatically on read-outs from many chemical pathology laboratories. A further formula is the National Kidney Foundation clinical practice guidelines formula.

Further reading

Stevens LA et al. (2006) Assessing kidney function – measured and estimated glomerular filtration rate. New England Journal of Medicine354: 2473–2483.

The effect of low-dose dopamine on renal blood flow has been questioned. The effect of increasing urine output is now thought to be largely due to the rise in cardiac output. Low-dose dopamine is still used and is not obsolete, as it often helps in shock whatever the mechanism.

Haem pigment casts obstruct the tubules.

A high-protein diet confers no advantage and should not be used. Always choose Kumar and Clark!

No, albumin infusion is not contraindicated but its effect is transient. It is sometimes used in diuretic-resistant nephrotic syndrome patients with an albumin of less than 20g/L. It is combined with diuretic therapy, e.g. furosemide. There is no good evidence, however, of its clinical usefulness.

Proteinuria sufficient to cause the nephrotic syndrome has been described with captopril. Angiotensin II receptor antagonists would be better in the circumstances you describe.

Further reading

Tryggvason K et al. (2006) Hereditary proteinuria syndromes and mechanisms of proteinuria. New England Journal of Medicine354: 1387–1401.

Expansion of the interstitial compartments (i.e. the peritoneal cavity in ascites) is secondary to the accumulation of sodium in the extracellular compartment. Sodium retention occurs because of increased Na /K – ATPase expression and activity in the cortical collecting duct. Additional factors include elevated tumour necrosis factor alpha (TNF-α) levels and an increase in circulating atrial natriuretic protein (ANP) levels, which change capillary permeability.

Acute nephritic syndrome with acute kidney injury causes hyperkalaemia. Nephrotic syndrome does not, unless acute kidney injury supersedes.

IVU shows the anatomical detail better than US and was regarded by many as first choice. US does not show pelvicalyceal anatomy as well but it does rule out major abnormalities, e.g. obstruction, and many urologists do not now use IVU. US followed by contrast-enhanced computed tomography has become more common.

1. Trimethoprim, an oral cephalosporin, or ciprofloxacin is used. A pretreatment urine culture should be obtained if possible and the treatment can then be changed according to bacterial sensitivities and clinical response.

2. Dose: amoxicillin 250mg every 8 hours for 5 days. Co-amoxiclav is safe in pregnancy. Bacteruria should always be treated in pregnancy and shown to be eradicated.

This depends on the clinical need. Intermittent catheterization is associated with fewer urinary infections. Bladder training involves closing off the catheter intermittently for increasing lengths of time.

Pulse-wave velocity is an indicator of arterial stiffness measured by Doppler ultrasound. Its use is not widespread but some studies suggest that it indicates atherosclerosis independent of blood pressure and might therefore be of prognostic value. The properties of the arterial wall, its thickness and the arterial lumen diameter are factors that influence PWV.

There is evidence to suggest that chronic hyperuricaemia causes nephropathy, but this does not happen as often as was originally thought. Renal disease

Aspirin in large doses used over a long time can produce analgesic nephropathy; this was well described in Australia some years ago. In small doses, e.g. 75–150mg a day, aspirin appears very safe and should be used for secondary prevention of further coronary events.

Renal lesions are rare and at this dose and frequency the patient is very unlikely to develop analgesic nephropathy.

Allopurinol blocks the enzyme xanthine oxidase which converts xanthine into urate. The level of urate in the blood falls, as does the amount in the urine. It does not cause uric acid stones.

In renal artery stenosis there is reduced renal perfusion, reduced transglomerular pressure and reduced glomerular filtration rate (GFR), which leads to acute renal failure. The response is intrarenal activation of the renin-angiotensin system, which leads to efferent arterial vasoconstriction. This restores transglomerular pressure and glomerular filtration rate. Angiotensin-converting enzyme (ACE) inhibition or blockade prevents angiotensin release and stops the resultant response. Use other drugs, such as nifedipine or a beta-blocker.

1. Duplex scanning compared to arteriography is over 90% sensitive and specific.

2. Yes, and this is now best practice for the diagnosis.

Small calculi might be missed.

This is a very specialized area and consultation with a paediatric urologist is essential. In general, hydronephrosis is being detected more frequently as routine ultrasonography becomes more common. In most cases, fetal surgery has not been beneficial. The most common cause of hydronephrosis is pelviureteric obstruction, which does not generally impair renal function. Expectant management with follow-up at 2-monthly intervals is the best approach.

In renal failure, oedema is due (as in other conditions) to fluid retention. The oedema is generalized but is often first noticed in the lax tissues around the eyes (periorbital area).

Blood is protein and therefore contains nitrogen, which is converted to urea; hence the rise in urea concentration with a gastrointestinal bleed. It is unclear whether sodium valproate does decrease the urea concentration but it does have a number of metabolic effects. Valproate produces anorexia, which reduces protein intake, and this could lower the serum urea. Of course, you also get a low urea in severe liver disease, which very rarely occurs with sodium valproate. Sodium valproate also raises the ammonia level, again rarely, which could affect the urea level.

BUN is shorthand for blood urea nitrogen; that is the blood urea. We now do not measure blood urea, we measure serum or plasma urea. There is, therefore, no difference between the BUN and the serum urea.

Small body mass.

There are many mechanisms but vasopressin levels are elevated so that free water and urea excretion are reduced. Angiotensin II and aldosterone are also increased, reducing sodium and hence water excretion.

Renal impairment is usually reversible but cases have been reported in which progression occurs when lithium has not been stopped immediately. It is uncommon if lithium therapy is monitored with serum levels.

CRF can present with polyuria, which is due to failure of tubular reabsorption. When depression of glomerular filtration occurs, Renal disease oliguria tends to replace polyuria. Because tubular dysfunction always accompanies glomerular disease to some extent, the urine output is not a useful guide to renal function. The oedema occurs because of increased sodium tubular reabsorption.

This is a term used for the appearance of the skin, literally ‘a frost’, which occurs only in terminal renal failure. In the age of dialysis and renal transplantation it is now not seen in developed countries.

Terlipressin has been most used and a response occurs in about 60% of patients, usually over a few days. It improves circulatory function by vasoconstriction of the dilated splanchnic arteries, which subsequently suppresses the activity of the endogenous vasoconstrictor systems, resulting in increased renal perfusion. The response, however, is frequently transient: most patients with the hepatorenal syndrome require liver transplantation.

ACE inhibitors reduce intraglomerular pressure and proteinuria as well as blood pressure in chronic renal failure. They slow progression of the renal disease (Box 11.1).

Further reading

Herbert LE (2006) Optimising ACE-inhibitor therapy for chronic kidney disease. New England Journal of Medicine354: 189–191.

If by ‘procedure’ you mean immunosuppressive regime, then for a high-risk patient (e.g. after a previous graft), CD25 monoclonal antibodies (e.g. basiliximab or dacluzimab) are used as induction therapy, followed by mycophenolate (replacing azathioprine) and tacrolimus.

Malignant transformation does not occur in PCKD.

Further reading

Perrone R (2006) Imaging progression in polycystic kidney disease. New England Journal of Medicine354: 2181–2183.

Prostate biopsy. A histological diagnosis is essential; the Gleason Scoring System, which guides treatment and includes prognosis, depends on this.

The risk of prostate cancer is approximately two-fold in men with first-degree relatives affected. There is perhaps a trend to an increase when other relatives are affected. In the particular instance of the 50-year-old man the correct procedure is rectal ultrasound-guided needle biopsy. The serum prostate-specific antigen (PSA) is useful in that:

• a PSA < 4 is normal

• a PSA 4.1–10 means the cancer is confined to the prostate

• a PSA 10 indicates the likelihood of extraprostatic extension by up to 30- to 40-fold.

Urinary retention can persist for days, particularly in elderly men with enlarged prostate glands. After 24 hours, catheterization is usually performed. Cholinesterase inhibitors are now not used because of side-effects.

1. Amyloid involvement of the kidneys produces enlarged, pale kidneys.

2. Giant cells are due to the fusion of activated macrophages and are seen in chronic inflammation, e.g. tuberculosis.

Normal people excrete 30mg of albumin in 24 hours. Excretion of 30–300mg is called microalbuminuria. Above 300mg in 24 hours protein can be detected by dipstix and is termed ‘albuminuria’.

Prerenal failure is due to hypovolaemia, hypotension or fluid and electrolyte depletion. You need, therefore, to replace fluids initially with 0.9% saline with potassium (20mmol). Monitor the pulse, blood pressure and venous pressure. A diuresis will occur when volume repletion has taken place. 11 113

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