Clinical use of diuretics

CME Renal Medicine
on therapy in renal disease. Arch Intern Med 1981;141:1039–41.
Richard S, Jothy S. A prospective study on Liam Plant MB MRCPI FRCPE, Consultant
the impact of the renal biopsy in clinical Renal Physician, Department of Renal management. Clin Nephrol 1986;26:217–21.
5 Cohen AH, Nast CC, Adler SG, Kopple JD.
Medicine, Cork University Hospital, Cork, Clinical utility of kidney biopsies in the ing directly inhibits sodium and chloride diagnosis and management of renal disease.
Am J Nephrol 1989;9:309–15.
Clin Med 2003;3:517–20
6 Farrington K, Levison DA, Greenwood RN, What are diuretics?
concentrating and diluting mechanisms.
ment and normal kidney size. Q J Med 1989;70: 221–33.
How do they work?
Diuretics are widely used in clinical med- Michael J. Knowledge of renal histologyalters patient management in over 40% of 1994;9:1255–9.
reabsorption at different sites along the 8 Tomson C, Porter T. Asymptomatic micro- which investigations for which patients? A Thiazide and related diuretics1–3 review of the evidence. BJU Int 2002;90:
Diuretics of another class, the thiazides 9 McGregor DO, Lynn KL, Bailey RR, Robson RA, Gardner J. Clinical audit of the use of used agents (Table 1).1–3 Although most renal biopsy in the management of isolated microscopic hematuria. Clin Nephrol 1998;
zone), are also organic anions secreted in 10 Nakao N, Yoshimura A, Morita H, Takada this site (eg acetazolamide) are of rela- distal tubule and connecting segment.
in non-diabetic renal disease (COOP-ERATE): a randomised controlled trial.
Lancet 2003;361:117–24.
11 Feehally J. Treating IgA Nephropathy – principle applies to the proximal tubular Who, When and How? Nephron Clin Pract 2003;93:C47–8.
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Risk of developing end-stage renal disease nation of these classes can be especially in a cohort of mass screening. Kidney Int 1996;49:800–5.
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14 Ball S, Cook T, Hulme B, Palmer A, Taube D. The diagnosis and racial origin of 394 patients undergoing renal biopsy: an associ-ation between Indian race and interstitialnephritis. Nephrol Dial Transplant 1997; 12:71–7.
Diuretics cause natriuresis in oedematous and hypertensive states
Dietary salt intake restriction is essential with diuretic use
Rapid adaptation by the tubule blunts the initial response to diuretic therapy
Application of pharmacokinetic and pharmacodynamic principles improves the
achievement of clinical objectives
Sequential nephron blockade is effective in advanced chronic renal failure and
heart failure
KEY WORDS: diuretics, heart failure, kidney, nephron, oedema, pharmacodynamics,
pharmacokinetics, potassium, sodium

Clinical Medicine Vol 3 No 6 November/December 2003
CME Renal Medicine
prescribe a reduction in dietary salt intake difficult to achieve. Unfortunately, many channels of the principal cells in the cor- inhibits the effect of aldosterone on the intake occurs because of addition in food Low glomerular filtration rate (GFR): but not losing weight is likely to have an When are diuretics indicated?
How are they most effectively
pathophysiological states (renal failure, Pharmacokinetics are important in initi- cardiac failure, hepatic failure, nephrotic ating natriuresis, pharmacodynamics in increased natriuresis until the patient has is excreted in the tubular fluid, consider- proximal tubule: many organic ions new desired steady state, particularly if threshold may be difficult in the presence Decreased bioavailability: furosemide and water requires an excess of excretion over intake. Dietary salt intake frequently exceeds 100 mmol/day (~6 g salt/day).
diuretic is not active. For example, to lose 650 mmol over and above that needed to balance daily intake. It is irrational not to Table 1. Diuretic agents.
Diuretic class
Principal site of action
**Indicated if sulphonamide hypersensitivity due to combination of loop and thiazide diuretics Consider in severe heart failure+Specific benefits in advanced heart failure Clinical Medicine Vol 3 No 6 November/December 2003
CME Renal Medicine
Are there other specific
more frequently will not help. In difficult indications?
patients, but not all patients benefit.
effect. This is principally a local response greater than three litres per day, restric- Metabolic alkalosis due to chloride Use of adequate dose more frequently: furosemide acts for about six hours.
Hyperuricaemia – tubular handling with heart failure, particularly with more acute renal failure (ARF),11 and are in fact more likely to increase the frequecy with Hypersensitivity reactions such as response to loop diuretics declines.
to diminish anticipated nephrotoxicity.
skin rashes and interstitial nephritis.
What are the side effects of
urea concentrations because of renal may cause fetal electrolyte disturbances.
mised, and diuretics enter breast milk.
Electrolyte disturbances, for example: 2 Brater DC. Pharmacology of diuretics.
3 Ellison DH. Diuretic drugs and the treat- Clinical Medicine Vol 3 No 6 November/December 2003
CME Renal Medicine
Bischoff I et al. Coadministration ofalbumin and furosemide in patients with 5 Agarwal R, Gorski JC, Sundblad K, Brater John Main MB ChB FRCP MD, Consultant
affect response to furosemide in patients Nephrologist, James Cook University with nephrotic syndrome. J Am Soc Nephrol 2000;11:1100–5.
6 Rudy DW, Voelker JR, Greene PK, Esparza FA, Brater DC. Loop diuretics for chronic Clin Med 2003;3:520–5
renal insufficiency: a continuous infusion is 7 Fliser D, Schroter M, Neubeck M, Ritz E.
Coadministration of thiazides increases the 15–30% of otherwise unselected patients efficacy of loop diuretics even in patients vascular disease.1 It is easy to find; in our unit, about 75% of cases selected only on treatment in severe heart failure: a ran- efferent arteriolar constriction which is 9 Cooper HA, Dries DL, Davis CE, Shen YL, Domanski MJ. Diuretics and risk ofarrhythmic death in patients with left ven- sure is reduced. This loss of GFR is inde- 10 Pitt B, Zannad F, Remme WJ, Cody R et al.
The effect of spironolactone on morbidity and mortality in patients with severe heartfailure. Randomized Aldactone Evaluation stenosis. The effect of these drugs is dose ered with a view to revascularisation.
11 Mehta RL, Pascual MT, Soroko S, Chertow mortality, and nonrecovery of renal func-tion in acute renal failure. Atheromatous renal artery stenosis (ARAS) is common in arteriopaths
All the clinical manifestations of ARAS have more common causes in arteriopaths
ARAS and chronic renal failure (CRF) often co-exist, but the CRF is not usually due
to the ARAS (and therefore not improved by revascularisation)
The role of intervention in preventing end-stage renal failure remains unclear
The response to intervention in hypertension is usually no better than mild
When pulmonary oedema is due to ARAS, the response to intervention can be
When acute oliguric renal failure occurs as a consequence of renal artery occlusion,
excellent renal recovery can occur after intervention
KEY WORDS: atheromatous renal artery stenosis, ischaemic nephropathy,
athero-embolic nephropathy, renovascular hypertension

Clinical Medicine Vol 3 No 6 November/December 2003



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