Glomerulonephritis & Vasculitis

An AKI that is not pre-renal and not obstructed. The finding that redirects everything is an active urinary sediment — blood and protein on the dipstick, with no catheter and no infection to explain it. That patient does not need more fluid; they…

AKI + blood and protein on dip = intrinsic renal disease, today

The pathway

1 · Dipstick every AKI

Blood and protein without a catheter, trauma or proven infection is the finding
It is the cheapest test in the hospital and it is routinely skipped
A catheter or a UTI can explain blood, so interpret it with the history
Send a urine protein:creatinine ratio and ask for microscopy for red cell casts

2 · Look for the extra-renal clues

Haemoptysis — pulmonary-renal syndrome
Rash, particularly palpable purpura
Arthralgia, sinus symptoms or epistaxis, red eyes
Weight loss, fevers, night sweats
Recent sore throat or skin infection in a younger patient

3 · Stop making it worse

Stop true nephrotoxins such as NSAIDs, and review contrast exposure
Review ACE inhibitors and ARBs — haemodynamically active, not nephrotoxic
Withhold them temporarily where clinically appropriate (NICE: consider this in vomiting, diarrhoea or sepsis), and record a restart plan
Review every drug — interstitial nephritis is a differential, and PPIs and antibiotics are common causes
Do not keep giving fluid to an AKI that is not responding; assess the fluid state properly
Catheterise and scan the bladder to exclude obstruction — do not assume

4 · Send the immunology TODAY

ANCA, anti-GBM, ANA and dsDNA, complement C3 and C4
Immunoglobulins and serum electrophoresis, hepatitis B and C, HIV as per local practice
ASO titre where post-infectious disease is plausible
The turnaround dictates when treatment can start, and the disease does not wait for it

5 · Image, and think about the chest

Renal ultrasound — size, obstruction, and whether a biopsy is feasible
CXR, and a CT chest if there is haemoptysis or a suspicion of alveolar haemorrhage
Anti-GBM disease and ANCA vasculitis both move fast; anti-GBM in particular is measured in days

6 · Refer, and say the words

Nephrology today. Communicate it precisely: AKI, with blood and protein on dipstick unexplained by catheter or infection, and concern for glomerulonephritis or vasculitis
Renal biopsy is usually the diagnostic step, and it is planned by nephrology
Treatment is immunosuppression, and plasma exchange in selected disease — specialist decisions
Rheumatology and respiratory where there are extra-renal features

Drugs

Drug	Dose	Route	Notes
NSAIDs and other true nephrotoxins	STOP	—	ACE inhibitors and ARBs are not nephrotoxins — they are haemodynamically active. Review them and withhold temporarily where clinically appropriate, with a restart plan. Review every drug for interstitial nephritis.
Corticosteroids	Per nephrology	IV / PO	The mainstay of induction in immune-mediated disease. Not started before nephrology are involved.
Plasma exchange	Per nephrology	Procedure	Used in selected disease, notably anti-GBM, where delay costs kidneys.

When to escalate

Haemoptysis with an AKI and an active sediment — pulmonary-renal syndrome, renal and respiratory today,Creatinine rising day on day with blood and protein on dip — nephrology now, not a morning referral,Hyperkalaemia, acidosis, uraemia or fluid overload — dialysis assessment; see the AKI pathway,Anti-GBM suspected — this moves in days; the referral is the same hour you think of it

Reference: KDIGO glomerular diseases guidance; NICE NG148 acute kidney injury; BSR/EULAR guidance on ANCA-associated vasculitis. Local nephrology pathways take precedence.

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