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← Renal indexChapter sections
Purpose and principlesIndications, selection and cautionsMethod and interpretationClinical next stepsRisks, monitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Renal history and examination

Renal · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Time-critical presentation

Anuria, pulmonary oedema, severe hyperkalaemia features, uraemic encephalopathy or pericarditis, septic obstruction, rapidly progressive nephritic illness, clot retention or a threatened dialysis access requires same-day senior renal or urological escalation after ABCDE stabilisation.

Purpose and principles

Use symptoms, risk factors, medicines and focused examination to distinguish acute from chronic kidney disease, detect obstruction or systemic nephritis and identify immediate physiological danger.

Renal presentations are often silent until a blood test changes. A disciplined history reconstructs baseline kidney function, the temporal relationship to illness and medicines, and whether the patient is losing volume, retaining salt and water, obstructed, or developing an intrinsic inflammatory process. The examination then tests physiology rather than attempting to diagnose histology at the bedside.

The classic pre-renal, intrinsic and post-renal framework is useful but not exclusive. Sepsis may cause vasodilatation, tubular injury and drug accumulation simultaneously; heart failure can produce total-body fluid excess with poor effective renal perfusion; obstruction can coexist with infection. Keep parallel hypotheses until urinalysis, serial biochemistry and imaging narrow them.

There is no universal empirical 'renal medicine' after examination alone. Fluids can harm congestion, diuretics can worsen true depletion, and antibiotics require source and renal-dose decisions. Immediate treatment is directed by verified physiology and the local AKI, sepsis, hyperkalaemia or obstruction pathway.

Key points

  • Start with time course and baseline: hours to days suggests acute kidney injury, whereas abnormalities persisting for at least three months support chronic kidney disease; an acute-on-chronic picture is common.
  • Quantify urine change rather than accepting 'passing less': ask usual and current volume, frequency, nocturia, stream, hesitancy, incomplete emptying, retention, catheter output and recent fluid losses.
  • Visible blood, froth, smoky urine, dysuria, flank pain, colic and fever localise different pathways. Painless visible haematuria still needs cancer-pathway assessment even when anticoagulated.
  • Ask about diabetes, hypertension, vascular disease, recurrent infection or stones, autoimmune symptoms, malignancy, pregnancy, recent sepsis, surgery, contrast, travel and family kidney history.
  • Reconcile every medicine and non-prescribed product: NSAIDs, ACE inhibitor or ARB, diuretics, antimicrobials, proton-pump inhibitors, lithium, calcineurin inhibitors, supplements and recreational drugs can change risk.
  • Volume assessment is a synthesis, not one sign. Weight trend, mucous membranes, capillary refill, pulse, lying and standing blood pressure, JVP, oedema and lung fields can disagree.
  • Look beyond the kidneys for mechanism: rash, purpura, synovitis, sinus or lung disease, neuropathy, haemoptysis, endocarditis stigmata and retinal changes can reveal systemic glomerulonephritis or vasculitis.

Indications, selection and cautions

Hypovolaemic or low-perfusion patternRed flag

Thirst, vomiting, diarrhoea, bleeding, poor intake or high-output stoma with weight loss, postural symptoms, cool peripheries and low JVP supports reduced effective perfusion, but beta-blockers and older age can blunt tachycardia.

Congested kidney patternRed flag

Rapid weight gain, orthopnoea, raised JVP, basal crackles, ascites and peripheral oedema suggest venous congestion or heart failure. Intravascular and interstitial volume cannot be inferred from ankle oedema alone.

Glomerular inflammatory patternRed flag

Smoky urine, oedema, hypertension, proteinuria, haematuria and reduced function, especially with purpura, arthritis, haemoptysis or sinus disease, suggests nephritic disease requiring prompt nephrology discussion.

Obstructive patternRed flag

Anuria, intermittent stream, hesitancy, palpable bladder, loin pain, pelvic malignancy, stones, recent instrumentation or neurogenic symptoms supports outflow or upper-tract obstruction. Sepsis plus obstruction is a drainage emergency.

Chronic uraemic pattern

Longstanding nocturia, pruritus, anorexia, nausea, restless legs, cognitive slowing, pallor, bruising, neuropathy and small kidneys or established complications suggest advanced chronic disease, though symptoms correlate imperfectly with eGFR.

Urological cancer signalRed flag

Painless visible haematuria, recurrent unexplained urinary bleeding, weight loss, persistent loin pain or a mass needs age- and symptom-specific NICE referral assessment; anticoagulation does not provide a sufficient explanation.

Method and interpretation

  1. 01
    Serial creatinine, eGFR, urea and electrolytesFirst step
    Why
    Establish direction, acuity and life-threatening biochemical complications.
    Interpretation and limitations
    Compare with all available baselines and urine output. Creatinine lags injury and eGFR is unreliable during rapid change; potassium, bicarbonate and sodium can dictate urgency before cause is known.
  2. 02
    Urinalysis with urine ACR
    Why
    Screen for blood, protein, infection, glucose and concentration, then quantify albumin loss.
    Interpretation and limitations
    Blood plus albumin and reduced function points toward renal parenchymal disease; nitrite or leucocytes require clinical and culture context. Dipstick protein misses lower-level albuminuria, so ACR remains necessary.
  3. 03
    Urine culture and microscopy when indicated
    Why
    Identify infection, cellular casts, crystals or a glomerular sediment.
    Interpretation and limitations
    Culture before antibiotics where this creates no harmful delay. Red-cell casts or dysmorphic cells support glomerular bleeding; absence of casts does not exclude active nephritis.
  4. 04
    Bladder scan and renal tract ultrasound
    Why
    Detect retention, hydronephrosis, kidney size and major structural disease without radiation.
    Interpretation and limitations
    A raised post-void residual supports lower-tract dysfunction. Early obstruction can precede dilatation, while chronic hydronephrosis may persist after relief; interpret with symptoms and function.

Clinical next steps

01Acutely unwellPhysiology before fine diagnosisFirst stepOliguria, rapid creatinine rise, hypotension, respiratory distress, confusion or suspected severe electrolyte disturbance.+
  1. 1Perform ABCDE, check observations, ECG and bedside glucose, obtain urgent U&E and venous blood gas, and measure actual urine output with a catheter only when indicated.
  2. 2Assess depletion versus congestion, stop or hold clearly unsafe medicines after indication review, and treat sepsis, hyperkalaemia, pulmonary oedema or shock through the appropriate protocol.
  3. 3Exclude obstruction promptly and seek nephrology or urology advice early for anuria, severe complications, unclear intrinsic AKI or failure to respond to initial treatment.
02Chronic abnormalityConfirm, classify and find causeIncidental low eGFR, albuminuria, persistent haematuria or known CKD without current physiological instability.+
  1. 1

Risks, monitoring and follow-up

  • Trend urine output, weight, blood pressure, oxygen requirement and examination rather than judging response from creatinine alone, which may change after the clinical event.
  • Repeat potassium and acid-base testing urgently when initially abnormal or when treatment, tissue breakdown, oliguria or a relevant medicine could change them quickly.
  • For chronic disease, record both eGFR and ACR trajectory and use the monitoring frequency in NICE NG203, increasing it after AKI or medicine changes.
  • Review all prescribed, over-the-counter and herbal products at every transition, documenting which were held, why, and the criteria and date for restarting.
  • Safety-net visible haematuria, falling urine output, breathlessness, swelling, fever with flank pain and uraemic symptoms with a specific route for urgent reassessment.

Special situations

Baseline is a diagnostic test

A creatinine of 150 micromol/L can represent stable CKD or a major acute rise in a person with low muscle mass. Retrieving prior results often changes the entire pathway.

Oedema is not intravascular volume

Nephrotic syndrome and heart failure can produce marked tissue oedema with low effective arterial volume. Fluid or diuretic decisions need the full circulatory picture.

Anticoagulation unmasks, not explains

Blood thinners may increase the visibility of urinary bleeding but do not remove the need to investigate an underlying tumour, stone, infection or glomerular lesion.

The bladder is part of renal examination

A painless palpable bladder or large residual can explain kidney impairment and may be missed when assessment focuses only on the loins and ankles.

Access protection starts early

A functioning fistula is the patient's lifeline. Avoid compression, arterial sampling or routine cannulation and escalate absent thrill, pain, bleeding or distal ischaemia.

Common pitfalls

  1. 01

    Calling every creatinine rise dehydration and giving fluid without checking congestion or obstruction.

  2. 02

    Using ankle oedema alone to decide that a patient is intravascularly overloaded.

  3. 03

    Omitting non-prescribed NSAIDs, supplements, injected therapies and recreational drugs from the medication history.

  4. 04

    Attributing visible haematuria to anticoagulation and failing to arrange cancer-pathway assessment.

  5. 05

    Ignoring urine output because creatinine has not yet risen after an acute insult.

  6. 06

    Writing 'renal review' without stating acuity, volume state, complications, mechanism or action.

Practice

Two practice questions

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Question 1 of 2
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RenalOriginal SBA

Visible haematuria on anticoagulation

An older adult taking apixaban reports painless visible haematuria twice this month and is otherwise stable. What is the best interpretation?

Choose one answer, then submit
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • NICE NG148 acute kidney injury recommendationsNational AKI recognition, assessment and escalation guidance.
  • NICE NG203 chronic kidney disease recommendationsCKD classification, investigation and referral criteria.
  • UK Kidney Association eCKD guideUK clinical approach to CKD assessment and management.
  • BAUS urological history and examination guideFocused urinary red flags and examination framework.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
Palpate for a distended bladder and examine for loin or graft tenderness. A normal abdominal examination does not exclude upper-tract obstruction, particularly when obstruction is early or unilateral.
  • In established kidney failure, inspect fistula or graft access without cannulating it casually, listen for a bruit where trained, and protect that limb from avoidable venepuncture and blood-pressure cuffs.
  • Finish with a one-line problem representation: acuity, urine output, volume/perfusion, likely pre-renal/intrinsic/post-renal mechanism, complications and the next action.
  • 05
    FBC, CRP, glucose, bone and liver profile
    Why
    Find anaemia, infection, diabetes, calcium disturbance and systemic contributors.
    Interpretation and limitations
    Normocytic anaemia can accompany CKD but blood loss, haemolysis, iron deficiency and marrow disease must be considered. Calcium and albumin results need context before attributing them to renal bone disease.
  • 06
    Targeted immunology and paraprotein screen
    Why
    Investigate systemic glomerular, vasculitic or monoclonal disease when the phenotype justifies it.
    Interpretation and limitations
    ANCA, ANA, complements, anti-GBM, immunoglobulins and serum free light chains are not indiscriminate panels. Discuss urgently when lung haemorrhage, rapidly falling function or heavy proteinuria is present.
    • Retrieve previous creatinine, ACR, blood pressure and imaging; confirm chronicity over at least three months while checking for a superimposed acute change now.
  • 2Classify by eGFR G category and ACR A category, review diabetes and cardiovascular risk, quantify progression and arrange ultrasound or serology only when guideline indications are present.
  • 3Address medicines and blood pressure, provide kidney-health and sick-illness advice, and refer using NICE/UKKA progression, albuminuria, haematuria, KFRE and diagnostic criteria.
    • 03Urinary tract symptomsSeparate infection, obstruction and malignancyDysuria, loin pain, lower urinary tract symptoms, visible blood or a palpable bladder.+
    1. 1Check stability, fever, sepsis, pain, retention and clots; obtain urinalysis and culture, creatinine and haemoglobin as clinically indicated.
    2. 2Use bladder scanning, ultrasound or CT selected for suspected retention, hydronephrosis or stone. Infected obstruction requires urgent decompression rather than antibiotics alone.
    3. 3Route unexplained visible or persistent non-visible haematuria through the current NICE cancer criteria while also assessing renal causes with ACR, blood pressure and function.