Renal system

CHAPTER 7 RENAL SYSTEM



Renal dysfunction in critical illness 184

Investigation of acute renal dysfunction 185

Oliguria 188

Management 188

Acute renal failure 189

Renal replacement therapy 190

Peritoneal dialysis 194

Outcome from acute renal failure in intensive care 195

Management of patients with chronic renal failure 195

Prescribing in renal failure 196

Plasma exchange 199


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




Prerenal failure


This refers to decreased glomerular filtration rate (GFR) due to reduced renal perfusion. There is no tubular damage. May be reversed by adequate fluid resuscitation and reperfusion of the kidney.



Acute tubular necrosis (ATN)


Decreased GFR is due to reduced perfusion, resulting in ischaemic renal tubular damage. There is no immediate reversal on restoration of perfusion, but it usually improves over time. This is the commonest pattern of ARF (requiring renal replacement therapy, e.g. haemofiltration) seen on ICU.



Acute cortical necrosis (ACN)


Total and irreversible loss of renal function results from severe prolonged ischaemia of kidneys. This is rare. It is seen occasionally in obstetric patients following placental abruption and haemorrhage where combination of a hypotension, hypercoagulable state and endothelial injury leads to thrombosis of renal vessels.



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.




History and examination



image Is there any indication of pre-existing renal disease? Vascular disease, diabetes, multisystem disease/vasculitis, chronic anaemia or previously abnormal U&Es are all suggestive. (Look for small shrunken kidneys on ultrasound or CT.)

image Is there any evidence for prerenal impairment, e.g. dehydration, hypovolaemia or hypotension?

image Is there any evidence for new intrinsic renal impairment, e.g. sepsis, nephrotoxic drugs?

image Is there any history or evidence of trauma or obstruction to the GU tract?


Investigations



Serum urea, electrolytes and creatinine


Serial measurements are used to monitor renal function and predict the need for renal replacement therapy. Avoid placing undue significance on single results. Take serial samples and look at trends.



Creatinine clearance


Creatinine clearance is a surrogate measure for glomerular filtration rate and may be required to guide dose reduction of drugs in renal failure. Creatinine clearance estimates are provided by a number of hospital laboratories based on formulae. These may, however, be misleading in critical illness, particularly where large fluid shifts and renal support are confounders. Formal assessment of creatinine clearance requires a 24-h urine collection, but may be extremely helpful. (See Prescribing in renal failure, p. 196.)



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:


image Urinary U&Es.

image Urine and plasma osmolality.

image Urine microscopy: are there casts, red cells, crystals?

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:



Creatine kinase (CK)/urinary myoglobin.

A raised serum creatine kinase and raised urinary myoglobin (early sign only) are indicative of rhabdomyolysis, for example following trauma, crush injury (see Rhabdomyolysis, p. 320.)



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


Imaging.

Plain abdominal films may show calcification or stones. Intravenous pyelogram (IVP) is not usually performed in ARF. Renal ultrasound may demonstrate small shrunken kidneys in cases with CRF and is useful to show obstruction (e.g. dilated ureters or renal pelvis). Although renal ultrasound is seldom indicated as an emergency investigation in the intensive care patient with renal failure, it should be a routine investigation during daylight hours to rule out renal obstruction or vascular causes.


CT scan with contrast may be useful in trauma/obstruction.


Renal biopsy and radioisotope perfusion scans may be useful in difficult cases.



OLIGURIA


Oliguria is defined as a urine output of less than 0.5 mL kg−1 h−1 for at least 2 consecutive hours. Most cases of oliguria do not progress to ARF if adequate steps are taken.


image Review the biochemistry results. Is there evidence of deteriorating renal function over time (i.e. increasing serum urea and creatinine)?

image Review the clinical status of the patient. Is there evidence of dehydration/hypovolaemia suggested by: thirst, poor tissue turgor (pinch skin on back of hand), dry mouth, cool pale limbs, large respiratory swing on arterial line, low CVP or low stroke volume index?

image Are CO and blood pressure adequate?

image Is there any obvious cause for renal failure, e.g. chronic renal insufficiency, nephrotoxic drugs, rhabdomyolysis?

image Is there an occult source of sepsis?


MANAGEMENT


Related posts:

Overdose, poisoning and drug abuse Introduction to intensive care Trauma Basic principles Respiratory system Practical procedures

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Jun 4, 2016 | Posted by in CRITICAL CARE | Comments Off on Renal system

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