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Renal Calculi and Nephrocalcinosis 373
Prevention of recurrence. Further treatment depends on the type of
stone and any underlying condition identified during screening investigations
(see Table 9.6). For prevention of all stones, whatever the cause, a high intake
of fluid (to produce a urine volume of 2–2.5 L/day) must be maintained,
particularly during the summer months. This is the mainstay of treatment
when no metabolic or renal abnormality has been identified (‘idiopathic
stone formers’).
• Idiopathic hypercalciuria. Patients should be encouraged to consume
a normal calcium diet and avoid foods containing large amounts
ofoxalate. A water softener may be helpful for patients who live
inhardwater areas. Thiazide diuretics, e.g. bendroflumethiazide,
reduce urinary calcium excretion and are used if hypercalciuria
persists.
• Mixed infective stones. Meticulous control of bacteriuria, if necessary
with long-term, low-dose, prophylactic antibiotics and a high fluid intake,
helps to prevent recurrent stone formation.
• Uric acid stones are prevented by the long-term use of the xanthine
oxidase inhibitor allopurinol, which allows the excretion of the more
soluble precursor compound hypoxanthine, in preference to uric acid.
Oral sodium bicarbonate supplements to maintain an alkaline urine, and
hence increased solubility of uric acid, are an alternative approach in
those patients unable to tolerate allopurinol.
• Cystine stones. A very high fluid intake (5 L of water in 24 hours) is
needed to maintain solubility of cystine in the urine. An alternative is
d-penicillamine, which chelates cystine, forming a more soluble
complex.
Nephrocalcinosis
Nephrocalcinosis is diffuse renal parenchymal calcification that is detectable
radiologically. The causes are listed in Table 9.7. It is typically painless and
hypertension and renal impairment commonly occur. Treatment is of the
underlying cause.
Table 9.7 Common causes of nephrocalcinosis
Mainly medullary Mainly cortical (rare)
Hypercalcaemia Renal cortical necrosis
Renal tubular acidosis
Primary hyperoxaluria
Medullary sponge kidney
Tuberculosis
374 Renal disease
URINARY TRACT OBSTRUCTION
The urinary tract may be obstructed at any point between the kidney and the
urethral meatus, resulting in dilatation of the tract proximal to the obstruction.
Dilatation of the renal pelvis is known as hydronephrosis. Eventually there is
compression and thinning of the renal parenchyma, with a decrease in size
of the kidney.
Aetiology
In adults the common causes are prostatic obstruction (hypertrophy or
tumour), gynaecological cancer and calculi (Table 9.8).
Clinical features
• Upper urinary tract obstruction results in a dull ache in the flank or loin,
which may be provoked by an increase in urine volume, e.g. high fluid
intake or diuretics. Complete anuria is strongly suggestive of complete
bilateral obstruction or complete obstruction of a single functioning kidney.
Table 9.8 Causes of urinary tract obstruction
Within the lumen
Calculus
Tumour of renal pelvis or ureter
Blood clot
Sloughed renal papillae (diabetes, NSAIDs, sickle cell disease or trait)
Within the wall
Congenital anomalies of the urinary tract (usually detected antenatally or in
infancy)
Stricture: ureteric or urethral
Neuropathic bladder
Pressure from outside the wall
Prostatic hypertrophy/tumour
Pelvic tumours
Diverticulitis
Aortic aneurysm
Retroperitoneal fibrosis (periaortitis)
Accidental surgical ligation of the ureter
Retrocaval ureter (right-sided obstruction)
Pelviureteric compression (bands; aberrant vessels)
Phimosis
NSAIDs, non-steroidal anti-inflammatory drugs.
Acute Kidney Injury 375
Partial obstruction causes polyuria as a result of tubular damage and
impairment of concentrating mechanisms.
• Bladder outlet obstruction results in hesitancy, poor stream, terminal
dribbling and a sense of incomplete emptying. Retention with overflow
is characterized by the frequent passage of small quantities of urine.
Infection commonly occurs and may precipitate acute retention of urine.
Depending on the site of obstruction, an enlarged bladder or hydronephrotic kidney may be felt on examination. Pelvic (for malignancy) and
rectal examination (for prostate enlargement) is essential in determining the
cause of obstruction.
Investigations
Imaging studies are performed to identify the site and nature of the obstruction and, together with serum creatinine, to assess function of the affected
kidney:
• Ultrasonography is the initial investigation but helical/spiral CT scanning
has a higher sensitivity for detecting calculi as well as details of the
obstruction. Excretion urography identifies the site of obstruction and
shows a characteristic appearance (a delayed nephrogram, which
eventually becomes denser than the non-obstructed side).
• Radionuclide studies (p. 13) are unhelpful in acute obstruction but may help
in long-standing obstruction, to differentiate true obstructive uropathy from
retention of tracer in a low-pressure unobstructed pelvicalyceal system.
• Subsequent investigations may include retrograde and antegrade
pyelography (p. 354), cystoscopy and pressure-flow studies during
bladder filling and voiding.
Management
Surgery is the usual treatment for persistent urinary tract obstruction.
Elimination of the obstruction may be associated with a massive postoperative diuresis, resulting partly from a solute diuresis from salt and urea
retained during obstruction and partly from the renal concentrating defect. In
some cases, definitive relief of obstruction is not possible and urinary diversion may be required. This may be simply an indwelling urethral catheter, a
stent placed across the obstructing lesion or the formation of an ileal conduit.
ACUTE KIDNEY INJURY
Acute kidney injury (AKI) is defined as an abrupt deterioration in renal function, usually over hours or days. It is usually (but not always) reversible over
a longer period of days or weeks. It may be associated with sudden, lifethreatening biochemical disturbances such as hyperkalaemia. The distinction
between AKI and CKD or even acute-on-chronic kidney disease is not always
obvious. AKI is usually recognized with a falling urine output and/or rising
376 Renal disease
Table 9.9 RIFLE classification for acute kidney injury
Grade Serum creatinine Urine output criteria
Risk
Injury
Failure
↑ SCr to ≥1.5 × from baseline
↑ SCr ≥2 × from baseline
↑ SCr ≥3 × from baseline or
SCr
≥350 μmol/L with an acute
increase
≥40 μmol/L
Loss
ESKD
AKI, acute kidney injury; ESKD, end-stage kidney disease; SCr, serum creatinine.
• Baseline SCr is considered to be within 1 week.
• When baseline SCr is not known and in the absence of a history of chronic kidney
• Only one criterion (SCr or urine output) has to be fulfilled to qualify for a stage.
• AKI should be both abrupt (within 1–7 days) and sustained (more than 24 hours).
Persistent AKI >4 weeks
Persistent renal failure >3 months
disease, calculate a baseline SCr using the Modification of Diet in Renal Disease
equation for assessment of kidney function, assuming a glomerular filtration rate of
75 mL/min/1.73 m2.
serum urea and creatinine. It is important to consider situations when urea
and creatinine are less accurate predictors of deteriorating renal function.
AKI may be:
1. Prerenal (reduced kidney perfusion, leading to a fall in GFR)
2. Renal (injury to the glomeruli, tubule or vessels)
3. Postrenal (urinary tract obstruction: functioning kidneys cannot excrete
urine. With back pressure affecting function).
The RIFLE criteria (Risk, Injury, Failure, Loss, End-stage renal disease)
(Table 9.9) help define AKI, by describing three levels of renal dysfunction
(R, I, F) and two outcome measures (L, E) associated with a rise in serum
creatinine or a decrease in urine output. These criteria indicate an increasing
degree of renal damage and have a predictive value for mortality.
The Acute Kidney Injury Network (AKIN) has proposed a modification of
the RIFLE criteria to include less severe AKI, a time constraint of 48 hours,
and gives a correction for volume status before classification.
• ‘R’ in RIFLE is stage 1 (a serum creatinine rise of ≥26.4 μmol/L, i.e. a
1.5-fold increase within 48 hours)
• ‘I’ is stage 2, (a two- to three-fold increase in serum creatinine)
• ‘F’ is stage 3, (an increase in serum creatinine of >300%, equal to
≥354 μmol/L).
Urine output data are the same.
<0.5 mL/kg/hour ≥6 hours
<0.5 mL/kg/hour ≥12 hours
<0.3 mL/kg/hour ≥24 hours
Acute Kidney Injury 377
Epidemiology
The incidence of AKI varies widely, depending on the population studied and
the definition used, e.g.:
• Community-acquired AKI on admission to hospital: approximately 5% in
the UK (superimposed on CKD in half of these)
• Severe AKI (creatinine >500 μmol/L, often requiring dialysis): about
130–140 per million population per year
• Approximately 50% of patients with septic shock will have AKI.
The outcome of AKI is variable. Uncomplicated AKI carries a good
prognosis with mortality rates <5%–10%. In contrast, AKI complicating nonrenal organ system failure (in the ITU setting) is associated with mortality rates
of 50%–70%, which have not changed for several decades. Sepsis-related
AKI has a significantly worse prognosis than AKI in the absence of sepsis.
Approaching AKI
Prerenal AKI. Falling renal blood flow leads to a reduction in GFR. This might
either be due to changes in the circulation or intrarenal vasomotor changes
that reduce glomerular perfusion pressures. Common causes with a falling
effective circulating volume include:
• Hypovolaemia of any cause, including dehydration or haemorrhage
• Hypotension without hypovolaemia, including cirrhosis or septic shock
• Low cardiac output, including cardiac failure or cardiogenic shock
• Any combination of the above.
Common intrarenal causes include:
• NSAIDs, ACE inhibitors, amphotericin B and calcineurin inhibitors, often in
the context of added changes in renal blood flow.
Autoregulation maintains glomerular filtration close to normal despite
wide variations in renal perfusion pressure and volume status. Once
autoregulation fails, GFR drops and AKI develops. Over time, reduced blood
flow may lead to established parenchymal injury – but if renal perfusion is
corrected early, AKI should resolve fully.
A few simple biochemical measures can help differentiate prerenal AKI
from intrinsic renal disease (Table 9.10). In prerenal AKI, urine specific gravity
or osmolality will rise, as solutes are concentrated into smaller urine volumes
(the kidney is retaining fluid to improve renal blood flow). Urine sodium will
be low due to salt retention but the fractional excretion of sodium (FENa) is a
more reliable measure of sodium retention.
Managing prerenal AKI largely depends on the underlying cause. Most
cases of AKI have an element of hypovolaemia, so prompt fluid resuscitation
is usually indicated. When uncertain as to the volume state of a patient, a
fluid challenge of 250 mL crystalloid will often prove whether hypotension
is fluid-responsive. Heart rate, blood pressure and urine output will all guide
response to resuscitation. See also cardiogenic shock (p. 558) and septic
shock (p. 561).
378 Renal disease
Table 9.10 Criteria for distinction between prerenal
and intrinsic causes of renal failure
Prerenal Intrinsic
Urine specific gravity
Urine osmolality (mOsm/kg)
Urine sodium (mmol/L)
Fractional excretion of sodium (Na+)
Fractional excretion of Na+ = urine [sodium] ÷ urine [creatinine] × 100
plasma [sodium] plasma [creatinine]
where [ ] is the concentration.
Postrenal AKI. In postrenal AKI, uraemia may result from obstruction
of the urinary tract at any point from the calyces to the external urethral
orifice. Commonly, however, it is due to bladder outflow obstruction (prostate
disease in men) or bilateral ureteric obstruction (stones or tumours). Almost
every case of unexplained AKI should be investigated with an ultrasound to
exclude obstruction, as once relieved (and if acute), renal function will return
to baseline.
Renal (parenchymal) AKI. This is most commonly (80%–90%) due to
acute tubular necrosis (ATN; see below and also Table 9.11). Almost any
cause of prerenal AKI, if prolonged to the point at which renal autoregulation
fails (see above), will lead to ischaemic ATN. If not ischaemic, then ATN
usually results from direct tubular toxins. As a result, ATN is common in
hospital practice. Other causes of parenchymal AKI include:
• Diseases affecting the intrarenal arteries and arterioles as well as
glomerular capillaries, such as a vasculitis, accelerated hypertension,
cholesterol embolism, haemolytic uraemic syndrome, thrombotic
thrombocytopenic purpura (TTP), pre-eclampsia and crescentic
glomerulonephritis.
• Acute tubulointerstitial nephritis. This also occurs when renal tubules
are acutely obstructed by crystals: e.g. after rapid lysis of certain
malignant tumours following chemotherapy (acute hyperuricaemic
nephropathy).
• Acute bilateral suppurative pyelonephritis or pyelonephritis of a single
kidney.
>1.020 <1.010
<20
<1%
>40
>1%
Clinical and biochemical features
The early stages of AKI are often completely asymptomatic. Although some
symptoms are attributable to uraemia, the manifestations of AKI are the result
of many different metabolic abnormalities.
Acute Kidney Injury 379
Table 9.11 Some causes of acute tubular necrosis
Haemorrhage
Burns
Diarrhoea and vomiting, fluid loss from fistulae
Acute pancreatitis
Diuretics
Myocardial infarction
Congestive cardiac failure
Endotoxic shock
Snake bite
Myoglobinaemia
Haemoglobinaemia (due to haemolysis, e.g. in falciparum malaria,
‘blackwater fever’)
Hepatorenal syndrome
Radiological contract agents
Drugs, e.g. aminoglycosides, NSAIDs, ACE inhibitors, platinum derivatives
Abruptio placentae
Pre-eclampsia and eclampsia
ACE, angiotensin-converting enzyme; NSAIDs, non-steroidal anti-inflammatory drugs.
• Alteration of urine volume. Oliguria usually occurs in the early stages.
Recovery of renal function typically occurs after 7–21 days and in the
recovery phase, which may last some weeks, there is often passage of
large amounts of dilute urine.
• Biochemical abnormalities include hyperkalaemia, metabolic acidosis
(unless there is loss of hydrogen ions by vomiting or aspiration of gastric
contents), hyponatraemia (due to water overload from continued drinking
after the onset of oliguria or administration of 5% glucose), hypocalcaemia
due to reduced renal production of 1,25-dihydroxycholecalciferol and
hyperphosphataemia due to phosphate retention.
• Symptoms of uraemia are weakness, fatigue, anorexia, nausea and
vomiting, followed by mental confusion, seizures and coma. There may
be pruritus and bruising. Breathlessness occurs from a combination
of anaemia and pulmonary oedema secondary to volume overload.
Pericarditis may occur in severe untreated uraemia and may be
complicated by a pericardial effusion and tamponade. Impaired platelet
function causes bruising and exacerbates gastrointestinal bleeding.
Infection occurs due to immune suppression.
380 Renal disease
Investigation of the uraemic emergency
The purpose of investigation, together with clinical examination, is three-fold:
1. To differentiate acute from chronic uraemia.
2. To document the degree of renal impairment and obtain baseline
values so that the response to treatment can be monitored. This is
accomplished by measurement of serum urea and creatinine.
3. To establish whether AKI is prerenal, renal or postrenal, and to
determine the underlying cause so that specific treatment (e.g.
intensive immunosuppression in granulomatosis with polyangiitis)
may be instituted as early as possible and thus prevent progression to
irreversible renal failure.
Investigations
• Urinalysis, urine microscopy, particularly for red cells and red cell casts
(indicative of glomerulonephritis), and urine culture. Urine should be
tested for free haemoglobin and myoglobin, where appropriate. Urine
PCR is helpful if parenchymal disease is possible.
• Blood tests including measurement of serum urea, electrolytes,
creatinine, calcium, phosphate, albumin, alkaline phosphatase
and urate concentrations. Full blood count and examination of the
peripheral blood film where necessary. Anaemia and a high erythrocyte
sedimentation rate (ESR) may suggest myeloma or a vasculitis
as the underlying cause. Coagulation studies, blood cultures and
measurements of nephrotoxic drug blood levels should be carried
outifappropriate.
• Renal ultrasound excludes obstruction and gives an assessment of
renal size; CT is useful for the diagnosis of retroperitoneal fibrosis and
some other causes of urinary obstruction, and may also indicate cortical
scarring.
• Renal biopsy should be considered in every patient with unexplained AKI
and normal-sized kidneys.
• Optional investigations (depending on the case):
• Serum protein electrophoresis for myeloma
• Serum autoantibodies, ANCAs and complement
• Antibodies to hepatitis B and C and HIV may suggest polyarteritis
(hepatitis B virus), cryoglobulinaemia (hepatitis C virus) or HIV as the
cause of AKI.
Management
The best form of management of AKI is prevention, e.g. by optimizing fluid
balance in hospitalized patients (p. 323) and ensuring volume expansion
in patients with impaired kidney function undergoing radiological contrast
studies. The principles of management of established AKI are summarized
Acute Kidney Injury 381
Emergency Box 9.1 Principles of management of a
patient with acute kidney injury
Emergency resuscitation
To prevent death from hyperkalaemia (p. 387) or pulmonary oedema.
Establish the aetiology and treat the underlying cause.
• History, including family history, systemic disease, use of nephrotoxic
drugs
• Examination includes assessment of haemodynamic status and, if
appropriate, pelvic and rectal examination
• Investigations (p. 380), which may include bladder catheterization or flush
of existing catheter to exclude obstruction
Prevention of further renal damage
Early detection of infection and prompt treatment with antibiotics. Avoid
hypovolaemia, nephrotoxic drugs, NSAIDs and ACE inhibitors.
Management of established renal failure
• Seek advice from a nephrologist
• Once fluid balance has been corrected, the daily fluid intake should
equal fluid lost on the previous day plus insensible losses (approximately
500 mL)
• Diet – enteral nutrition is preferred over parenteral; sodium and potassium is restricted
• Nursing care, e.g. prevention of pressure sores
• Adjust doses of drugs that are excreted by the kidney, and monitor serum
drug levels where appropriate (refer to a national formulary for guidance)
• Monitor daily: serum biochemistry, fluid input and output and body weight
to assess fluid balance changes
• Frequent review regarding the need for dialysis
Careful fluid and electrolyte balance during recovery phase
Large volumes of dilute urine may be passed until the kidney recovers its
concentrating ability.
ACE, angiotensin-converting enzyme; NSAIDs, non-steroidal anti-inflammatory drugs.
in Emergency Box 9.1. Hypovolaemia (prerenal) and obstruction (postrenal)
must be excluded as contributing factors in all patients. Early specialist
review is advisable. With patients often requiring management in a highdependency setting. Good nursing, infection control and physiotherapy are
vital. Fluid balance, as intake and output (particularly urine output), will be
key to recovery. Daily weights, lying and standing blood pressure, medication
review to withhold nephrotoxins, collateral history and past results will all
382 Renal disease
Table 9.12 Indications for dialysis and/or haemofiltration in AKI
Progressive uraemia with encephalopathy or pericarditis
Severe biochemical derangement, especially if there is a rising trend in an
oliguric patient and in hypercatabolic patients
Hyperkalaemia not controlled by conservative measures
Pulmonary oedema
Severe metabolic acidosis: pH <7.1
For removal of drugs causing the AKI, e.g. gentamicin, lithium, severe aspirin
overdose
AKI, acute kidney injury.
form part of the management plan. Dialysis and haemofiltration are sometimes necessary; they do not hasten recovery from AKI but are performed
as a bridge while patients are receiving treatment for the underlying cause
or there is a natural improvement in kidney function. Indications for dialysis
are listed in Table 9.12. Whether haemodialysis, haemofiltration or peritoneal
dialysis (p. 388) is used depends on the facilities available and the clinical
circumstances.
Prognosis
Prognosis depends on the underlying cause. The most common cause of
death is sepsis as a result of impaired immune defence (from uraemia and
malnutrition) and instrumentation (dialysis and urinary catheters and vascular
lines). In patients who survive, renal function usually begins to recover within
1–3 weeks. AKI is irreversible in a few patients. This is probably due to cortical necrosis as unlike tubules, which regenerate, the cortices heal with the
formation of scar tissue.
CHRONIC KIDNEY DISEASE
Chronic kidney disease (CKD) implies long-standing, and usually progressive, impairment in renal function. It is defined on the basis of persistent
(>3 months) evidence of kidney damage (proteinuria, haematuria or anatomical abnormality) and/or impaired GFR (Table 9.13). Patients at risk of CKD,
e.g. with diabetes mellitus or hypertension, should be regularly screened to
look for evidence of disease.
Aetiology
Causes of CKD vary depending on geographical area, racial group and age.
Diabetes mellitus, hypertension and atherosclerotic renal vascular disease