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Summary Renal medicine summaries

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  • The University Of Edinburgh (ED)

Summary notes for renal medicine. Contains information about clinical features of each condition, as well as relevant diagnostic tests and investigations, risk factors, causes and management guidelines. Everything has been cross referenced with passmedicine or Zero to finals and management is ref...

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Document information

  • November 20, 2023
  • 22
  • 2023/2024
  • Summary

Subjects

  • renal
  • kidneys
  • medicine
  • clinical medicine
  • pharmacology
  • anatomy
  • summary

Written for

  • The University of Edinburgh (ED)
  • Unknown
  • (MBCHB)

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saskiahogan

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ACUTE KIDNEY INJURY



CLINICAL SIGNS PATHOPHYSIOLOGY
Often asymptomatic Not a diagnosis – clinical syndrome
Pre-renal - Increase in serum creatinine
- Cold peripheries, weak pulse, tachycardia o > 26 micromol/L in < 48 hours
- Hypotension (relative to baseline) o > 50% rise from baseline within last 7
- Reduced skin turgot days
- Dry mucous membranes or
Renal/post-renal - Urine volume < 0.5ml/kg/hr for 6 hours
- Cold peripheries, tachycardia eGFR not accurate for assessment of AKI where there
- Hypertension, increased JVP are rapid changes in creatinine
- 3rd heart sound, bibasal crepitations
- Oedema RISK FACTORS
Check for enlarged bladder Elderly
Signs of systemic disease: purpuric rash, joint Existing comorbidities: CKD, HF, DM, HTN, vascular
swelling disease, urological disease
Hx of AKI
INVESTIGATIONS Medications: Anti-HTNs, ACEi/ARBs, NSAIDs
- Urinalysis
- In absence of infection: blood + protein 
glomerulonephritis/vasculitis
- High specific gravity indicates CAUSES
concentrated urine 1. Pre-renal failure
- Bloods a. Effective circulating volume depletion:
o Hb often normal dehydration, haemorrhage, sepsis,
o Raised WCC/CRP in cardiac failure
infection/inflammation 2. Renal failure
o Low platelets – marrow problem or a. Renovascular disease: renal artery
HUS thrombosis/embolus, HUS
- Calcium – hypercalcaemia directly toxic to b. Glomerular disease: RPGN, vasculitis
tubules c. Tubulointerstitial: ATN, AIN
- CK 3. Post-renal failure
- Plasma protein electrophoresis – Bence a. Bladder outlet: BPH, bladder tumour,
Jones protein ureteric stricture, blocked catheter
- ANCA, Anti-GBM, ANA b. Ureteric: pelvi-ureteric obstruction,
- Blood, urine cultures stones/clot, cancer
ECG if K+ > 6 Renovascular + glomerular disease typically present
CXR with increased BP and increased ECF
Bladder scan, USS



MANAGEMENT
Fluids
- Haemodynamically unstable  resuscitate with up to 2L
- Dehydration/postural hypotension more cautious fluid challenge
- Euvolaemic  monitor and replace urine output
- Hypervolaemic  restrict fluids +/- IV diuretics or dialysis
Catherisation if suspicion of BOO
Drugs:
- Stop nephrotoxic drugs
- Withhold drugs likely to exacerbate low eGFR
- Dose adjustment according to severity of renal failure
Hyperkalaemia (K+ > 6.5 or ECG changes)
- 30ml 10% calcium gluconate to protect myocardium
- Oxygenate, 10mls salbutamol nebuliser, 10 units actrapid in 50ml 50% dextrose
- Remove K+: urine, potassium binder, dialysis
- Monitor K+ and glucose

,RENOVASCULAR DISEASE



LARGE VESSEL OCCLUSION PATHOPHYSIOLOGY
Main renal artery thrombosis/embolus Renal cause of AKI
- Must be bilateral to cause AKI (or unilateral Typically presents with volume expansion
if single functioning kidney)
- Oliguria/anuria
- Mild loin pain (if any)
- Doppler USS/CT angio shows lack of renal
SMALL VESSEL OCCLUSION – CHOLESTEROL
blood flow EMBOLI
Renal cause of AKI
Revascularisation rarely able to save renal
function Common after arterial procedures (e.g. coronary
angiogram)
Often associated with eosinophilia
MICROANGIOPATHIC HAEMOLYTIC
O/E: may see ischaemia of the toes, often with
ANAEMIA
relatively well-preserved pulses
Presenting feature of small vessel renal disease
Biopsy would show cholesterol emboli in small
- HTN vessels leading to the kidney
- Thrombocytopenia
- Haemolysis: schistocytes on blood film
o Raised LDH
o Raised unconjugated bilirubin HAEMOLYTIC URAEMIC SYNDROME
o Low haptoglobin Generally seen in young children
Renal biopsy: glomerular microthrombi – capillary Produces triad of
loops are occluded with microthrombi so GFR is 1. AKI
low 2. Microangiopathic haemolytic anaemia
Can be caused by 3. Thrombocytopenia
- HUS Most are secondary: Shiga toxin-producing E. coli,
- Thrombotic thrombocytopenic purpura pneumococcal infection, HIV, SLE, drugs, cancer
- Systemic sclerosis Primary HUS (atypical) is due to complement
- Malignant HTN (typically SBP > 200mmHg) dysregulation
Treatment is supportive (no role for abx despite
preceding diarrhoeal illness in many patients)

, ACUTE INTERSTITIAL NEPHRITIS



CLINICAL SIGNS PATHOPHYSIOLOGY
AKI/clinically silent Immune-mediated disorder characterised by acute
- Reduction in renal function over weeks  inflammation affecting the tubule-interstitium of the
months kidney
- Urine output often preserved, may have
polyuria/nocturia Most commonly an allergic drug reaction most
o Although GFR is reduced, the common, but can be autoimmune. Looks the same as
injured tubules aren’t able to acute rejection of a kidney transplant
reabsorb salt and water as well as
normal leading to leakage of salt Toxins can also cause AIN – plant toxics, chemical
and water toxins, autotoxins from myeloma kidney
- Normally euvolaemic, normotensive
- Urinalysis bland, may see leukocytes
- May have eosinophilia
Often requires biopsy to confirm diagnosis CAUSES
In immune AIN there may be other features such Drugs
as rash, peripheral eosinophilia - Penicillin
May have: - NSAIDs
- Modest proteinuria - PPIs
- Urine may contain WCCs and WC casts - Mesalazine (delayed)
- Eosinophils present in up to 70% patients Infections
- Pyelonephritis
- TB
INVESTIGATIONS - Leptospirosis
- Hantavirus
Renal biopsy – evidence of intense inflammation
with infiltration of tubules and interstitium by Immune
polymorphonuclear leucocytes and lymphocytes. - Autoimmune disease
Eosinophils may be observed - Transplant disease
Often granulomas are evident, especially in drug- Sarcoidosis
induced AIN or sarcoidosis
Toxic – myeloma light chains, mushrooms



MANAGEMENT
Stop offending drug if possible
Consider steroids to accelerate resolution
Infection = abx
Immune = immunosuppression
Sarcoidosis = steroids

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