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CHAPTER13 Renal medicine and urology
Chronic kidneydisease
Slow d renal function over months/ years. Common (prevalence 8.5%); i with
age; ♀ > ♂. Usually asymptomatic. May be associated with i BP. In later stages
may cause nausea/ vomiting, anorexia, lethargy, oedema, dyspnoea, ± itching.
Causes
• DM
• i BP
• Urinary tract obstruction
• Chronic pyelonephritis
• Nephrotoxic drugs
Classication of CKD Figure 13.1 (E p. 411). Both i ACR and d
eGFR are associated with i risk of adverse outcomes (renal failure and
CVD). In combination, risk is multiplied.
Testing forCKD
• i BP
• DM (all type 2; type 1 if present >5y)
• CVD (stroke, TIA, IHD, heart failure, peripheral vascular disease)
• Structural renal tract disease, recurrent renal calculi, or BPH
• Multisystem disease with potential kidney involvement, e.g. SLE
• FH of end- stage kidney disease or hereditary kidney disease
• If prescribed drugs known to be nephrotoxic, e.g. calcineurin inhibitors
(e.g. ciclosporin, tacrolimus), lithium, NSAIDs
0 Repeat test in <2wk if eGFR <60mL/ min/ 1.73m2 and no previous test.
Frequency of CKD monitoring
testing to the individual according to underlying cause of CKD, eGFR/
ACR history, co- morbidities/ general health status, intercurrent illness, and
changes in drug treatment.
Investigation ofhaematuria E p. 420
Refer forrenal USS If:
• eGFR of <30 mL/ min/ 1.73m2 (G4/ 5) or accelerated progression of
CKD:sustained d in eGFR of ≥25% and a change in GFR category in
<12mo, or sustained d in eGFR of ≥15mL/ min/ 1.73m2 per year
• Symptoms of urinary tract obstruction
• Family history of polycystic kidney disease and aged >20y
Table13.3 Frequency ofCKD monitoring based oneGFR and
ACR levels
eGFR category ACR category
G1 ≤1×/ y 1×/ y ≥1×/ y
G2 ≤1×/ y 1×/ y ≥1×/ y
G3a 1×/ y 1×/ y 2×/ y
G3b ≤2×/ y 2×/ y ≥2×/ y
G4 2×/ y 2×/ y 3×/ y
G5 4×/ y ≥4×/ y ≥4×/ y
• CVD
• i Ca
• Polycystic kidneys
2+
• Glomerulonephritis
• Renovascular disease
• Interstitial nephritis
• SLE
N
Check eGFR + ACR (in most cases 1×/ y) if ≥1 of:
• AKI (E p. 412)
• Haematuria (E p. 420)
N
Table 13.3. Tailor frequency of
A1 A2 A3
• Amyloid
• Myeloma
• PAN
• AKI
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CHRONIC KIDNEYDISEASE
Management ofCKD Discuss causes of CKD, risks (progression of
renal disease, i BP, CVD, i mortality) and management:
• Treat reversible causes if possible; stop/ avoid nephrotoxic drugs (e.g.
NSAIDs). Consider d dose of other drugs as excretion/ metabolism
may be impaired. 0 Stop metformin if eGFR <30mL/ min/ 1.73m
• Annual review of CVD risk— check lipid prole; lifestyle advice
(smoking, weight d, exercise, alcohol consumption)— E p. 219
• Treat i BP (E p. 219)— target <140/ 90mmHg; if CKD + DM or CKD
+ ACR ≥70mg/ mmol, aim for BP <130/ 80mmHg
• Oer ACE inhibitor/ ARB if CKD + DM + ACR ≥3mg/ mmol; CKD +
iBP + ACR ≥30mg/ mmol; or CKD + ACR ≥70mg/ mmol
• Oer atorvastatin 20mg nocte (d CVD events and death by 20%). i
dose if <40% d in non- HDL cholesterol and eGFR ≥30mL/ min/ 1.73m2.
If eGFR <30mL/ min/ 1.73m2, seek specialist advice
• Oer folic acid/ vitamin B12 supplements if d on laboratory testing/
poor diet
2
Refer To renal physician if:
• eGFR <30mL/ min/ 1.73m2 or ACR ≥70mg/ mmol (unless caused by DM
and already treated) or ACR ≥30mg/ mmol + haematuria (unless urgent
referral for suspected cancer is indicated— E p. 420)
• Sustained d in eGFR of ≥25% + change in GFR category or sustained d
in eGFR of ≥15mL/ min/ 1.73m2 in <12mo
• Poorly controlled BP despite ≥4 antihypertensive drugs
• Known/ suspected rare/ genetic causes of CKD or renal artery stenosis
If renal outow obstruction Refer to urology.
Dialysis Starts if GFR <10– 15% normal. Needed lifelong unless transplant
becomes available. Refer to the patient’s renal unit if any problems.
• Haemodialysis Blood ows opposite dialysis uid and substances
are cleared along a concentration gradient across a semi- permeable
membrane. Problems:pulmonary oedema; infection (hepatitis, bacteria);
U&E imbalance; BP i or d; problems with vascular access; dialysis
arthropathy (especially shoulders and wrists); aluminium toxicity; time
• Continuous ambulatory peritoneal dialysis (CAPD) Permanent catheter is
inserted into the peritoneum via sc tunnel. Dialysis uid is introduced and
kept in the peritoneum; changed up to 5×/ d at home. Patient is not tied to a
dialysis machine. Problems:emergency referral— peritonitis, catheter blockage;
other problems— weight i, poor DM control, pleural eusion, leakage
Renal transplantation Usually sited in an iliac fossa. 5y graft survival
is ~88% for adults. Closer genetic matches l i survival rates. Problems:
• Rejection
• Persistent i BP
• Atherosclerosis (5× i risk MI
death) and i cholesterol
• Renal artery stenosis at 3– 9mo post- op
• Obstruction at ureteric anastomosis
• Ciclosporin- induced nephropathy
• Infection 2° to immunosuppression
• Malignancy from immunosuppressants
Further information
NICE (2014, updated 2015)Chronic kidney disease in adults. M www.
nice.org.uk/ guidance/ cg182
NICE (2013) Acute kidney injury. M www.nice.org.uk/ guidance/ cg169
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CHAPTER13 Renal medicine and urology
Specific kidneydiseases
Interstitial nephritis Important cause of renal failure. Associated with
inammatory cell inltration of the renal interstitium/ tubules. Causes:
• Acute interstitial nephritis Idiosyncratic reaction to drugs (penicillin,
NSAIDs, furosemide), or infection (Staphylococcus or Streptococcus)
• Chronic interstitial nephritis Idiopathic (most), drugs, sickle cell disease,
analgesic nephropathy
Presentation and prognosis Presents with AKI/ CKD, fever, arthralgia, eosinophilia. Patients with AKI have good prognosis. Those with CKD tend to
gradual deterioration over time.
Diabetic nephropathy E p. 325
Analgesic nephropathy Caused by prolonged heavy use of anal-
gesics (including NSAIDs). Presents with an interstitial nephritis- like picture.
Associated with i incidence UTI. Carcinoma of the renal pelvis is a rare
complication. Investigate promptly if the patient develops haematuria.
Glomerulonephritis Types and presentation— Table 13.4. Refer all
suspected cases urgently to a renal physician. Terminology:
• Focal— some glomeruli aected
• Diuse— all glomeruli aected
• Segmental— part of each glomerulus aected
• Global— all of each glomerulus aected
Chronic pyelonephritis Presents as CKD or one of its complications.
Probably arises from UTIs, vesico- ureteric reux, and consequent renal
scarring in childhood (E p. 856). Refer to a renal physician.
Table13.4 Types ofglomerulonephritis
Type Features
Minimal change Most common in children. Presents with nephrotic
Membranous 30% adult nephrotic syndrome. Underlying malignancy in
Focal segmental
glomerulosclerosis
Membranoproliferative
Proliferative Presents with nephritic syndrome. Classically seen 2wk
IgA disease (Berger’s
disease)
Rapidly progressive/
crescentic
syndrome
10% of adults. 1 in 3 enter remission, 1 in 3 are proteinuric,
1 in 3 progress to end- stage renal disease (ESRD)
Proteinuria or nephrotic syndrome. May be associated with
heroin misuse. >50% progress to CKD
50% present as nephrotic syndrome. Associations—
endocarditis, C3 nephritic factor (autoantibody),
hepatitisC, measles
after streptococcal infection. Prognosis is excellent
Causes recurrent haematuria in young men. Asimilar
histological picture is seen in Henoch– Schönlein purpura
(E p. 500). 30% progress to ESRD
Presents with haematuria, oliguria, i BP, acute kidney
injury. Vigorous treatment may preserve renal function.
Causes:anti- glomerular basement membrane disease
(Goodpasture’s disease), Wegener’s granulomatosis,
Henoch– Schönlein purpura
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SPECIFIC KIDNEYDISEASES
Haemolytic uraemic syndrome Most common cause
of AKI in children. Usually follows gastroenteritis. Due to E.coli
toxin. Have a high index of suspicion in any child with bloody
diarrhoea. Occasionally occurs without diarrhoea. Other features:
• Dehydration
• Oliguria (though may be polyuria)
• Proteinuria/ haematuria
• Haematological features— anaemia,
thrombocytopenia ± purpura
Management Admit for specialist care— often including dialysis. If associated with diarrhoeal illness, >80% make full recovery. Mortality is 1.8%.
Poor prognostic indicators are age >5y at onset and dialysis for >2wk.
Disease in the absence of diarrhoea has poorer prognosis.
• CNS symptoms— irritability,
drowsiness, ataxia, coma
• i BP (associated with non-
diarrhoeal disease)
Adult polycystic kidney disease Autosomal dominant disease (1 in
1000). Cysts develop in the kidney causing gradual d in renal function.
Common cause of CKD. Presents with haematuria, UTI, abdominal mass
(30% have cysts in the liver/ pancreas too), lumbar/ abdominal pain, and/ or
i BP. May be associated with mitral valve prolapse, and SAH/ berry aneurysms. USS shows large kidneys with multiple cysts. Refer to a renal physician
if CKD 3– 5. Treat infections and i BP. Check family members (though cysts
may not be seen <30y). 45% progress to ESRD by 60y.
Medullary sponge kidney Developmental abnormality of the medul-
lary pyramids of the kidney, characterized by dilatation of renal collecting
tubules. ♂ > ♀. There may be a family history. Most are asymptomatic and
the condition is an incidental nding. If symptomatic, presents with UTIs,
renal stones, haematuria. Refer if symptomatic. Usually prognosis is very
good and most require no treatment.
Renal vein thrombosis (RVT) Causes:nephrotic syndrome (15– 20%
develop RVT); membranous glomerulonephritis (30%); acute dehydration.
Presentation varies from no symptoms to severe pain and loin tenderness.
Suspect in at risk individuals if unexplained loss of renal function and RBCs
in urine. Refer to a renal physician for further investigation.
Renal artery stenosis Causes:atheroma, bromuscular hyperplasia (in
the young). Presents with i BP (may be severe or drug resistant); vascular
disease elsewhere; abdominal bruit; i Cr, d eGFR and proteinuria. If bilateral or extensive, renal failure may be precipitated by dehydration, dBP or
drugs (ACE/ ARB initiation; NSAID). Refer to a renal physician (if diagnosis
is unsure) or vascular surgeon (if diagnosis is known).
Alport’s syndrome X- linked or autosomal disease. Congenital sensori-
neural deafness, haematuria, proteinuria, and renal failure. Associated with lens
abnormalities, platelet dysfunction, and i BP. Causes ESRD by 3rd decade in
♂; ♀ rarely develop ESRD. Renal failure does not recur after transplantation.
Patient support and information
The National Kidney Federation F 0800 169 0936 M www.kidney.org.uk
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CHAPTER13 Renal medicine and urology
Renalstones
12% of ♂ and 3% of ♀ will develop a renal stone at some point; peak age
20– 50y. Symptoms are not dependent on size of the stone.
Riskfactors
• Family history— i risk ×3. Specic conditions:X- linked nephrolithiasis,
cystinuria, hyperoxaluria
sponge kidney
• Metabolic disease— e.g. gout, hypercalcaemia/ hypercalciuria, cystinuria,
renal tubular acidosis or other acidosis (ileostomy, adenomatous polyp),
oxaluria, aminoaciduria
• Dehydration • Immobilization • Chronic UTI
Drugs predisposing patients to stone formation Acetazolamide, allopurinol,
aspirin, steroids, indinavir, nelnavir, loop diuretics, probenecid, quinolones,
sulfonamides, theophylline, thiazides, triamterene, antacids, calcium/
vitamin D supplements, high- dose vitamin C.
Presentation Usually presents with pain ± nausea/ vomiting. Location
and type of pain gives clues about the site of the stone:
• Loin pain— kidney stone
• Renal colic— ureteric stone
Renalcolic
• Symptoms Severe pain with waves of i severity. Usually starts abruptly
as ank pain which then radiates around the abdomen to the groin as
stone progresses down the ureter. May be referred to testis/ tip of penis
in man or labia majora in women
• Signs Patient is obviously in pain— usually unable to sit still and keeps
shifting position to try to get comfortable (in contrast to peritonitis
where patients tend to keep still). May be pale and sweaty. May be mild
tenderness on deep abdominal palpation or loin tenderness, although
often minimal signs. If fever suspect infection
Other presentations UTI, haematuria, retention, renal failure (rare).
Dierential diagnosis Pyelonephritis; ruptured AAA; cholecystitis;
pancreatitis; appendicitis; diverticulitis; obstruction; strangulated hernia;
testicular torsion; pethidine addiction.
Immediate investigations Dipstick urine if possible. Absence of
RBCs does not exclude renal colic but consider alternative diagnosis.
Immediate management Stones usually pass spontaneously. Give
pain relief (diclofenac 75mg IM/ 100mg PR) ± antiemetic. Consider admission to hospital if:
• Fever
• Oliguria
• Poor intake of uid
• Pregnant
• Lives alone
• Uncertain diagnosis
If not admitted Encourage i uid intake; sieve urine for stones.
Monitor/ review pain relief and for complications.
Further investigations Can wait until the next working day and include:
• Strangury— bladder stone
• Interruption of ow— urethral stone
• Analgesia ineective/
short- lived
• Symptoms >24h
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RENALSTONES
• Blood U&E, creatinine, eGFR, Ca2+, PO
acid, albumin
• Urine M,C&S; RBCs. Consider checking ‘spot’ test for urine cystine, and
ACR, Ca2+, PO
• Radiology X- ray of kidneys, ureters, and bladder— 90% of renal
3−
, uric acid, and sodium excretion
4
3−
, alkaline phosphatase, uric
4
stones are radio- opaque— only urate and xanthine stones are radiotranslucent; renal tract USS
Follow- up 50% recur in 5– 7y. Give general advice on prevention of
stones (Table 13.5). If investigations show any loss of renal function, renal
obstruction, or remaining stones— refer to urology. Dependent on composition of stones, give dietary advice/ refer to dietician (Table 13.5).
Hyperoxaluria May be 1° (autosomal recessive condition) or 2° to gut
resection/ malabsorption or dietary excess of spinach or vitamin C. Take
specialist advice on management. There are 2 types of 1° hyperoxaluria:
• Type 1 hyperoxaluria Calcium oxalate stones are widely distributed
throughout the body. Presents as renal stones and nephrocalcinosis in
children. 80% have chronic renal failure in <20y
• Type 2 hyperoxaluria More benign but less common— nephrocalcinosis
but no chronic renal failure
Cystinuria Most common aminoaciduria. Usually presents with stones at
age 10– 30y. Urine:cystine i, ornithine i, arginine i, lysine i. Take specialist
advice on management.
Hypercalcaemia E p. 336
0 Hypercalciuria may occur without hypercalcaemia and is found in ~80%
of patients with calcium oxalate stones.
Table13.5 Prevention ofrenal stones
Type of stone Preventative measures
All types i uid intake (>2– 2.5L/ 24h) especially in hot weather;
Calcium oxalate Urinar y alkalinization with potassium citrate; avoid
Calcium phosphate Low Ca2+ diet; avoid vitamin D supplements.
Staghorn/ triple
phosphate (calcium,
magnesium, and
ammonium)
Urate Avoid beer as has uricosuric eect; allopurinol; urinary
Cystine Urinary alkalinization with potassium citrate
dweight if obese; d animal protein and i fruit/ vegetables
in diet; d salt intake
chocolate, tea, rhubarb and spinach, nuts, beans, beetroot;
d citrus fruits; bendroumethiazide 2.5mg od may help if
hypercalciuria; hyperoxaluria is treated with pyridoxine
Bendroumethiazide 2.5mg od may help if hypercalciuria
Associated with UTI due to Proteus spp. and urinary
stasis, e.g. due to anatomical abnormality. Treat UTI with
antibiotics
alkalinization with potassium citrate (pH >6.5)
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CHAPTER13 Renal medicine and urology
Haematuria, bladder and renalcancer
Haematuria
on urine dipstick is signicant. Causes:Table 13.6.
• May be visible (frank) or non- visible (microscopic— up to 20% of the
population). Non- visible haematuria (NVH) may be symptomatic (e.g.
dysuria, i frequency) or non- symptomatic (usually found by chance)
• Investigate all cases of haematuria:check BP; palpate the abdomen;
send MSU for M,C&S
• Free Hb and myoglobin make urine test sticks +ve in absence of red
cells. Urine discolouration can also result from beetroot ingestion,
porphyria, bilirubinuria 2° to biliary obstruction or drugs, e.g. rifampicin
• If cause is identied (e.g. sample taken when menstruating, UTI)—
repeat the check for blood in urine once treated/ resolved
Refer urgently tourology To be seen in <2wk if:
• Child with unexplained haematuria; consider admission if unwell
• Age ≥45y with unexplained visible haematuria without UTI or visible
haematuria that persists/ recurs after successful treatment of UTI
• Age ≥60y with unexplained NVH + dysuria or i WCC on blood test
Further primary care investigation If urgent referral not indicated:
• Check renal function:urine sample for ACR; blood for eGFR
• Consider PSA testing + DRE for ♂ with visible haematuria
• Refer for pelvic USS if ♀, age ≥55y, visible haematuria + unexplained
vaginal discharge, d Hb, i platelets or i blood glucose
• Refer for renal USS if visible or persistent NVH (on >1 urine sample)
Non- urgentreferral
• Urology/ gynaecology— age ≥60y + recurrent/ persistent UTI
• Urology— any age + unexplained visible or symptomatic NVH, or age
≥40y and asymptomatic NVH
• Nephrology— eGFR <30mL/ min/ 1.73m2 or evidence of declining
eGFR; signicant proteinuria (ACR ≥30mg/ mmol); age <40y with
isolated haematuria (without proteinuria) + i BP; visible haematuria
coinciding with intercurrent infection (usually URTI)
0 If ongoing persistent NVH without proteinuria/ CKD, follow- up 1×/ y
with BP, urine dipstick for haematuria, ACR, and eGFR until resolves.
Table13.6 Causes ofhaematuria
Infection UTI, urethritis, prostatitis, TB, schistosomiasis, infective endocarditis
Tumour Bladder, prostate, kidney or endometrial. Wilm’s tumour (E p. 884)
Inammation GN, Henoch– Schönlein purpura, IgA nephropathy, Goodpasture’s
Structural Stones (renal, bladder, ureteric), cysts (simple cysts, polycystic renal
Blood Sickle cell disease, coagulation disorders
Trauma Surgery/ catheter/ foreign body, sexual activity, abdominal/ back injury
Drugs Sulfonamides, cyclophosphamide, NSAIDs
Others Menstruation, fabricated/ induced illness
N
Blood in the urine. Detected on urine dipstick. ≥1+ blood
syndrome, polyarteritis, post- irradiation
disease), BPH, congenital vascular anomalies
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HAEMATURIA, BLADDER AND RENALCANCER
Sterile pyuria White cells in the urine without UTI. Repeat with clean
catch MSU. If persists, refer to urology. Causes:
• Inadequately
treated UTI
• Appendicitis
• Calculi
• Prostatitis
• Bladder tumour
• Renal TB
• Papillary necrosis
• UTI with failure to
culture organism
• Interstitial nephritis or
cystitis
• Polycystic kidney
• Chemical cystitis, e.g.
due to radiotherapy
Bladder cancer Incidence: ~11,000 cases/ y in the UK; ♂:♀ 85:2.
Transitional cell carcinoma (TCC) is most common in the UK— squamous
cell carcinoma (SCC) is most common worldwide. Risk factors:smoking (½
male cases are attributable to smoking); aromatic amine exposure (textile
or rubber industries); stasis of urine; chronic UTI; schistosomiasis (SCC).
Presents with haematuria. Less commonly:recurrent UTI, frequency, pelvic
or loin pain, and/ or bladder outow obstruction.Investigation and manage-
ment MSU— excludes UTI and detects sterile pyuria; check urine dipstick
for NVH. Refer to urology to be seen in <2wk. Treatment depends on
stage at diagnosis— Table 13.7.
Table13.7 Stage ofbladder cancer, treatment, and prognosis
Stage Description and treatment Prognosis
T1
Disease conned to mucosa/ submucosa. Treated
(80%)
with transurethral resection of the tumour
(TURBT) ± single intravesical chemotherapy
T2 Invasion into connective tissue around the bladder.
Treatment is with TURBT ± radiotherapy
T3 Invasion through muscle into the fat layer. Treated
with radical cystectomy and/ or radiotherapy
T4 Spread beyond the bladder. TURBT for local
symptoms, palliative radio- ± chemotherapy
Very good— most
die from other
causes
60% survive 5y
40– 50% 5y survival
20– 30% 5y survival
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Investigation and management Urine:RBCs. Blood:i PCV (2%), anaemia,
hypercalcaemia. Radiology:USS, CXR. Refer to urology to be seen in <2wk.
Treatment includes surgery where possible ± chemo- , radio- , and/ or biological therapy. Overall 50% 5y survival.
Hypernephroma Clear cell adenocarcinoma of renal tubular epithe-
lium. Incidence: 9300 cases/ y in the UK. Typical age: 50y. ♂:♀ 81.5:1.
Spread can be local or haematogenous (bone, liver, lung— causes cannon
ball metastases seen on CXR). Presentation:haematuria, abdominal mass,
loin pain, anaemia, left varicocele (♂) and, occasionally, night sweats.
Further information
NICE (2014, updated 2015)Chronic kidney disease in adults. M www.
nice.org.uk/ guidance/ cg182
NICE (2015, updated 2017)Suspected cancer:recognition and referral. M
www.nice.org.uk/ guidance/ ng12
Information and support forpatients
Cancer Research UK F 0808 800 4040 M www.cancerresearchuk.org
Macmillan Cancer Support F 0808 808 0000 M www.macmillan.org.uk
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CHAPTER13 Renal medicine and urology
Urinary tractinfection
Urinary tract infection (UTI) is one of the most common conditions seen in
general practice accounting for up to 6% of consultations (1 case/ average
surgery). ♀ > ♂. 20% of women at any time have asymptomatic bacteriuria and 20– 40% of women will have a UTI in their lifetime.
Infecting organisms E. coli (>70%), Proteus spp., Pseudomonas spp.,
streptococci, staphylococci.
Riskfactors
• Prior infection
• DM
• Stones
• Pregnancy
• Dehydration
Presentation ofUTI
• Cystitis Frequency, dysuria, urgency, strangury, low abdominal pain,
incontinence of urine, acute retention of urine, cloudy or oensive
urine, and/ or haematuria
• Pyelonephritis Loin pain, fever, rigors, malaise, vomiting, and/ or haematuria
Dysuria and urgency Painful micturition resulting from urethral or bladder
inammation. Causes:UTI, urethral syndrome, inammation (e.g. interstitial cystitis, radiation- induced cystitis), intravesical lesion (tumour, stone),
atrophy (menopause).
Frequency Passage of urine more often than usual. Causes:
• UTI
• Urethral syndrome
• Detrusor instability
• Inammation (e.g. interstitial
cystitis)
• Fibrosis (e.g. post- radiotherapy)
• Atrophy (menopause)
• Neurogenic bladder (e.g. MS)
Initial investigation If uncomplicated UTI in an otherwise healthy ♀,
test urine with a leucocyte and nitrite dipstick. If +ve treat for UTI. Reasons
to send MSU for M,C &S:
• Unresolved infection after
antibiotics
• Recurrent UTI
• Uncatheterized ♂ with UTI
• Catheterized ♂ or ♀ with
symptomatic UTI
• Impaired renal function
0 Take MSU prior to starting antibiotics— send to the laboratory fresh.
Further investigation Consider further investigation with blood tests
(eGFR ± PSA if >40y and ♂) and/ or radiology (e.g. renal tract USS) if:
• GU instrumentation
• Catheterization
• d oestrogen
(menopause)
• Sexual intercourse
• External pressure (e.g. pregnancy,
broids)
• Bladder tumour or stone
• Enlarged prostate
• Drugs (e.g. diuretics)
• DM
• Excessive uid intake
• Habit
• Child— E p. 856
• Pregnant ♀— E p. 798
• Suspected pyelonephritis
• Haematuria— microscopic or
macroscopic— always investigate
further— E p. 420
• Abnormal renal tract
• GU malformation
• Urinary stasis (e.g.
obstruction)
• Delayed micturition
(e.g. on long journeys)
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URINARY TRACTINFECTION
• UTI in a ♂
• UTI in a child (E p. 856)
• Recurrent UTI in a ♀
• Unclear diagnosis (e.g. persisting symptoms but negative MSU)
• Pyelonephritis
• Unusual infecting organism
• Sterile pyuria (E p. 421)
Management
• Catheterized patients— E p. 427
• Pregnant ♀— E p. 798
All other patientsN Symptomatic relief with paracetamol ± NSAIDs. i uid
intake. Prescribe oral antibiotics, e.g. nitrofurantoin MR 100mg bd or trimethoprim 200mg bd (consider local guidelines/ resistance):
• 3d course for ♀ with uncomplicated UTI— consider delayed
prescription if mild symptoms
• 7– 10d course for ♂ or if GU malformation, immunosuppression,
relapse (same organism), or recurrent UTI (dierent organism)
Use a 7d course of a quinolone (e.g. ciprooxacin 250– 500mg bd) for pyelonephritis. Refer to urology if abnormalities are detected on further investigation or unable to resolve symptoms. Admission is rarely needed.
• Children— E p. 856
Prevention ofrecurrent cystitis Reinfection after successful treat-
ment of infection (90%) or relapse after inadequate treatment.
• General advice Advise to urinate frequently; i uid intake; double void
(i.e. go again after 5– 10 min) and void after intercourse
• Prophylactic antibiotics Consider prescribing either postcoitally (e.g.
nitrofurantoin MR 100mg stat) or continuously (trimethoprim 100mg or
nitrofurantoin 50mg nocte)
• Men with BPH Finasteride/ dutasteride and/ or doxazosin d UTI
• HRT Topical oestrogen d recurrent UTI in ♀ of all ages
• Vaccines Results of large- scale trials are awaited
Prostatitis E p. 430
Chronic pyelonephritis E p. 416
Urethral syndrome Symptoms of cystitis with −ve MSU. Unknown
cause. Associated with cold, stress, nylon underwear, COC, and intercourse. Advise uids ++ and to wear cotton underwear. Consider changing/ stopping COC, or trying topical oestrogen if postmenopausal.
Tetracyclines (e.g. doxycycline 100mg bd for 14d) or azithromycin (500mg
od for 6d) are helpful in some. If not settling, refer to urology.
Interstitial cystitis Predominantly middle- aged ♀. Can cause brosis of
the bladder wall. Main symptoms:frequency, urgency, and pelvic/ suprapubic
pain especially when the bladder is full. Often misdiagnosed as recurrent
UTI. MSU:no bacteriuria. Refer to urology for conrmation. There is no
satisfactory treatment although antispasmodics, amitriptyline and bladder
stretching under GA may help some patients.
Further information
NICE Antimicrobial prescribing:
• UTI (lower) (2018). M www.nice.org.uk/ guidance/ ng109
• UTI (recurrent) (2018). M www.nice.org.uk/ guidance/ ng112
• Acute pyelonephritis (2018). M www.nice.org.uk/ guidance/ ng111
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