Renal system

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CHAPTER 7 RENAL SYSTEM

RENAL DYSFUNCTION IN CRITICAL ILLNESS

Renal dysfunction is common in the ICU and frequently occurs as part of a syndrome of multiple organ failure. The cause of renal dysfunction is often multifactorial. Pre-existing renal impairment may be worsened by the effects of critical illness, including release of cytokines, activation of inflammatory cascades, hypoperfusion, altered tissue oxygen delivery and extraction, and altered cellular function. In addition, many drugs used in intensive care are predictably nephrotoxic, while others have been implicated in idiosyncratic nephrotoxic reactions.

Classically, the causes of acute renal dysfunction are divided into prerenal (inadequate perfusion), renal (intrinsic renal disease) and postrenal (obstruction). These are summarized in Box 7.1.

Box 7.1 Causes of renal dysfunction*

Pre-renal Renal Post renal
Dehydration Renovascular disease Kidney outflow obstruction
Hypovolaemia Autoimmune disease Ureteric obstruction
Hypotension SIRS and sepsis Bladder outlet obstruction (blocked catheter)
  Hepatorenal syndrome  
  Crush injury (myoglobinuria)  
  Nephrotoxic drugs  

* In many patients the cause of renal failure will be multifactorial.

Clinically, renal dysfunction is usually manifest as oliguria progressing to anuria, and so water retention is a key feature, although high-output renal failure, in which there are large volumes of poorly concentrated urine, may also occur. Renal dysfunction is associated with a reduction in creatinine clearance, and an accumulation of toxic molecules within the patient including potassium, urea, so called middle molecules and drug metabolites.

Three terms are commonly used in relation to different patterns of renal dysfunction/failure

INVESTIGATION OF ACUTE RENAL DYSFUNCTION

In many cases, the causes of acute renal dysfunction in the ICU can be determined from knowledge of the clinical background of the patient, and by simple history and examination. Most cases of ARF will prove to be prerenal or ATN. Up to 10% of cases, however, will have other significant underlying pathologies.

Investigations

Urinary biochemistry

Urine output should be monitored hourly. A low urine output should alert suspicion, but is not pathognomonic of renal failure. Urine output should be interpreted in the context of urinary biochemistry. Three simple investigations are helpful in distinguishing prerenal from intrinsic renal failure:

Normal urine osmolality depends on the patient’s hydration status, and may vary from hypo-osmolar (less than normal plasma osmolality 280 mosmol/L) to highly concentrated hyperosmolar (> 1000 mosmol/L).

In prerenal failure, the kidney functions maximally to retain sodium and water in order to re-expand plasma volume. The urine sodium concentration is low and the urine is maximally concentrated, as indicated by high osmolality (600–900 mosmol/L), and a urine to plasma urea ratio greater than 10.

As ATN develops, the renal tubules are no longer able to function normally, and are unable to retain sodium or concentrate the urine. The urinary sodium rises, urinary osmolality falls, and the urine to plasma urea ratio also falls. Eventually the urinary sodium and osmolality approach that of plasma. Renal tubular debris or casts may be seen in the urine. The distinguishing features of prerenal and renal failure are summarized in Table 7.1.

Table 7.1 Distinguishing features of prerenal and renal failure

  Prerenal Renal (ATN)
Urinary sodium* <10 mmol/L >30 mmol/L
Urinary osmolality* High Low
Urine: plasma urea ratio >10:1 <8:1
Urine microscopy Normal Tubular casts

* If patients have received diuretics, urinary sodium and osmolality are difficult to interpret.

Other investigations may be indicated depending on circumstances:

Vasculitis screen.

Renal disease may be associated with autoimmune conditions and vasculitis. An autoimmune/vasculitis screen may be appropriate, particularly in the presence of coexisting pulmonary disease. Seek advice. Investigations are listed in Table 7.2.

Table 7.2 Investigations for autoimmune disease in renal failure

Vasculitis Antineutrophil cytoplasmic antibodies (ANCA)
Goodpasture’s syndrome Antiglomerular basement membrane antibodies
Systemic lupuserythematosus (SLE) Antinuclear antibodies (ANA)Anti-double-stranded DNA antibodies
Rheumatoid disease Rheumatoid factor

MANAGEMENT

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