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Nephrology, Dialysisand Transplantation Postgrad Med J (1993) 69, 516-546 © The Fellowship of Postgraduate Medicine, 1993 Postgrad Med J: first published as 10.1136/pgmj.69.813.516 on 1 July 1993. Downloaded from Reviews in Medicine Nephrology, dialysis and transplantation K. Farrington1 and P. Sweny2 'Lister Hospital, Stevenage and 2Royal Free Hospital, London, UK Nephrology 1. Urine microscopy Pathogenesis of ARF Careful phase contrast microscopy of freshly Changes in renal haemodynamics are a feature of prepared urine sediment is one of the simplest, all types ofARF irrespective ofprecipitating insult. cheapest and most helpful investigations in neph- Recent studies have examined the role of rology and urology, but it is often omitted or endothelium-derived vasoactive factors in these delegated to the routine microbiology laboratories.1 changes. It should be the first investigation in all cases of haematuria or suspected glomerular disease. The Endothelin Endothelin is a 21-amino acid pep- rapid identification of red cell casts or dysmorphic tide. It is the most potent vasoconstrictor yet red cells can point the clinicians in the direction of discovered, being ten times more potent than renal biopsy and away from cystoscopy and angiotensin II. It has many other properties includ- arteriography.2 Doctors investigating renal pa- ing effects on ion transport, eicosanoid synthesis, tients should have access to a centrifuge and a good and renin and atrial natriuretic peptide (ANP) quality phase contrast microscope. With phase release. The renal vasculature appears particularly copyright. contrast, damaged or distorted red cells can easily susceptible to its vasoconstrictive effect. Renal be recognized (dysmorphic red cells).3 The ex- vascular resistance is increased by an effect on both tremes of osmolarity experienced with passage afferent and efferent arterioles. It also reduces the along the nephron may be important in producing glomerular ultrafiltration coefficient by inducing dysmorphic cells. Dysmorphic cells may have mesangial cell contraction.5 Thus both renal blood gained entry to the urinary tract via a ruptured flow and glomerular filtration rate (GFR) are glomerular basement membrane in an inflamed compromised (Table I). Factors known to increase glomerulus or through a ruptured tubular base- its production rate include hypoxia, shear stress, http://pmj.bmj.com/ ment membrane damaged by interstitial inflam- endotoxin, thrombin, adrenalin, neuropeptide Y, mation. The injury sustained during this passage is and interleukin 1. Many of these factors are thought more likely to account for their variable thought to be important in the pathogenesis of and abnormal morphology.4 If all the red cells are ischaemic ARF. Endothelin may well have a of a similar size and shape and well preserved, the pathogenic role in this setting. In support of this, haematuria is more likely to have been caused by a circulating levels of endothelin have been found to lesion below the nephron. Urological workup is be elevated in patients with ARF.6 Experimentally, on September 30, 2021 by guest. Protected then appropriate. monoclonal antibodies to endothelin and specific non-peptide endothelin antagonists have been 2. Acute renalfailure (ARF) found to protect against the development of post- ischaemic renal damage.7'8 Anti-endothelin anti- Progress in this area has centred on efforts to clarify bodies also protected against endotoxin-induced the pathogenesis of ARF and on the development falls in GFR3. of a variety of potential treatments most of which remain experimental. In the clinical setting, con- Endothelium-derived relaxing factor (EDRF) tinous modes of renal replacement therapy have Vasodilatation in response to acetylcholine and become routinely available for the treatment of bradykinin is mediated by a diffusible EDRF, ARF in the intensive care unit. In spite of this, the which has subsequently been identified as nitric mortality remains high. oxide. Its synthesis is catalysed by nitric oxide synthase from L-arginine, and blocked by the Correspondence: P. Sweny, M.A., M.D., F.R.C.P., arginine analogue L-NMMA. There are two Department of Nephrology and Transplantation, Royal enzyme systems, one constitutive, and responsible Free Hospital, Pond Street, London NW3 2QG, UK. for the physiological production ofEDRF, and the NEPHROLOGY, DIALYSIS AND TRANSPLANTATION 517 Postgrad Med J: first published as 10.1136/pgmj.69.813.516 on 1 July 1993. Downloaded from Table I Effects of endothelin and EDRF on renal onstrated in the amelioration of radiocontrast haemodynamics induced renal impairment19 and post-transplant ARF.20,21 Endothelin EDRF ANP alone, or in combination with dopamine, Renal blood flow Decreased Increased protects against post-ischaemic ARF.22,23 The Glomerular filtration rate Decreased No change effect of the drugs in combination appears no Afferent resistance Increased Decreased greater than the effect of ANP alone,24 in spite of Efferent resistance Increased Decreased the prevention, by dopamine, of the hypotensive Glomerular ultrafiltration Decreased ?Increased response to ANP. Loop diuretics produced long- coefficient term improvement in renal function after an ischaemic insult, perhaps by reducing the propor- tion of nephrons obstructed by Tamm-Horsfall protein cylinders.25 other inducible, and responsible for prolonged Most studies of therapy in experimental ARF EDRF production in some pathological circums- have concentrated on attempts to modify the tances. In addition to its vasodilator effect, nitric haemodynamic processes involved in the initiation oxide inhibits platelet adhesion and aggregation. In of the condition. Agents which stimulate regenera- these two actions, nitric oxide and prostacyclin tion ofdamaged tubules may also have therapeutic potentiate each other. EDRF also reduces the potential. Epidermal growth factor is one such release of renin and ANP9. Infusion of L-NMMA agent. It is a potent growth promoter to renal produces hypertension implying a physiological tubular cells, and has been found to accelerate role for EDRF in the maintenance ofnormal blood recovery in mercuric chloride-induced ARF in pressure.'1 Endothelium-derived nitric oxide also rats.26 exhibits profound effects on glomerular haemodynamics,7 L-NMMA inducing increased renal vascular resistance, decreased renal blood flow, with little effect on GFR (Table I). In Clinical Therapy in ARF is firmly based on post-ischaemic ARF, the vascular responses to aggressive resuscitation and optimization ofhaem- copyright. acetylcholine and bradykinin are blunted, suggest- odynamic parameters, attempts to nullify or re- ing impaired release of EDRF. " Haemoglobin and verse the precipitating insults, the appropriate use myoglobin are both potent inhibitors ofEDRF,'2'l3 of loop diuretics and low-dose dopamine, and the and this action may be important in the early institution of renal replacement therapy pathogenesis of ARF associated with haemolysis should sufficient renal function not be restored by and rhabdomyolysis. On the other hand, endotoxin these former measures. Continuous modes of renal and cytokines can stimulate the inducible nitric replacement have become standard in this situa- oxide synthase to produce a sustained burst of tion, especially for patients managed in intensive http://pmj.bmj.com/ EDRF, with resulting vasodilatation and resis- care units. There is very little controlled informa- tance to vasoconstrictor agents characteristic of tion comparing different modes oftherapy, but the septic shock. Administration of L-NMMA to rats firm clinical impression is that continuous treat- with septic shock produced improvements in blood ments have considerable advantages over intermit- pressure, renal function, and survival.'4 There is tent treatments particularly with respect to the also some limited clinical experience with the use of maintenance of haemodynamic stability, the de- L-NMMA in and of metabolic control and the septic shock.'5 gree stability on September 30, 2021 by guest. Protected capacity to provide optimal nutrition. A recent controlled trial has reported a significant benefit of Treatment of ARF pump-driven haemofiltration (continuous veno- venous haemofiltration-CVVH) over spontaneous Experimental Calcium antagonists have a num- arteriovenous haemofiltration (CAVH). Mortality ber of potentially beneficial effects on the com- in the CVVH group was less than in the CAVH promised kidney. These include antagonism of group in spite of a comparable degree ofcontrol of preglomerular vasoconstriction, reduction in cel- uraemia apparently based on serum creatinine lular calcium uptake in response to cell injury, and levels. Mortality was inversely related to the a possible action as a free radical scavenger.'6 volume of ultrafiltrate.27 It was suggested that Protective effects against the development of ARF differences in 'middle molecule' clearance resulting have been demonstrated in experimental models of from the differences in ultrafiltration volume might a number of different types of ARF including explain the effect. However, static biochemical post-ischaemic'7 and toxic.'8 Studies have been parameters often provide a poor assessment of the extended into the clinical setting, in which protec- adequacy of renal replacement treatments (vide tive effects of calcium antagonists have been dem- infra). 518 K. FARRINGTON & P. SWENY Postgrad Med J: first published as 10.1136/pgmj.69.813.516 on 1 July 1993. Downloaded from 3. Glomerulonephritis curately gauged from initial
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