Nephrology Notes

Nephrology

Haematuria

Indications for escalating investigations in haematuria:

..NICE say to refer to urology if painless macroscopic haematuria, more than forty years with persistent UTI, more than fifth with explained microscopic haematuria, if you can palpate a mass linked to a urinary tract.

..Refer to renal: eGFR going down quicker than would expect with age, significant amount of protein in urine = ratio >50, HTN with ?renal cause, frank haematuria and infection.

..Complications of cystoscopy: infection, abdo pain, incontinence, haematuria, bladder spasm

Proteinuria

..Definition: excess protein in urine. Normal <1.5g per day. Significant proteinuria is greater than 1g per day.

..US stats: men more than women, as more likely to be renal patients.

..likely to be transient. Dip again. Three consecutiverefer.

..Does affect certain ethnic groups: Blacks have high incidence of glomerular disease.

..Aetiology: 4 types. 1) transient 2) orthostatic 3) persistent due to extra-renal disease (normal renal function) 4) due to renal disease, persistent

1. Transient: doesn’t indicate any underlying renal disease, really low protein output, no there when test again, normal BP, no casts, no oedema. Causes: fever, exercise.

2. Orthostatic: thin, young adolescents, adults under thirty, prolonged standing – not in morning on urine sample, then have proteinuria at night. take urine samples before exercise to avoid transient proteinuria sampling.

3. Persistent, need three positive samples on dipstick to say this. Extra-renal, so BP normal etc. no oedema. Causes: overproduction of plasma proteins e.g. amylase in pancreatitis, Bence-Jones proteins in myeloma, haemoglobin after haemolytic anaemia, myoglobin after rhabdomyolysis.

4. Persistent due to renal disease, more than 500mg/day in urine. Active=casts, bland=nothing special in sediment. Lipids in urine, oedema, hyperlipidaemia, hypertension. Causes: macroscopic and microscopic causes of proteinuria.

..Primary=defect in basement membrane.

..Secondary=damage due to system disease

..Symptoms:

• Asymptomatic

• transient might have a hx of fever or exercise

• urine appearance (frothy)

• swelling in ankles, periorbital, genital.

..Exam: check fluid status. Signs of systemic diseases. BP and palpate kidneys.

..Ix: urine, bloods, imaging, biopsy.

..Urine & Bloods: Urinalysis & microscopy would do 3 times if you want to show it’s persistent. Dipstick very sensitive if macroalbuminuria, not good in microalbuminuria. 24-hour urine collection to quantify urine protein and also you would do a creatinine:protein ratio. Look for proteins, casts, bacteriuria. Early morning/later split collection looking for orthostatic. General renal disease bloods, immunology if ?rheumatology. Hep B causes nephrotic syndrome.

..Imaging: kidney ultrasound

..Biopsy: persistent proteinuria, abnormal imaging, haematuria, more than 1g per day of protein or reduced renal function.

..If necessary can do plasmapheresis.

..CXR if cardiac enlargement, sarcoid, ‘cannonball’ metastases from kidney cancer.

..PHAROAH for nephritic syndrome:

• Proteinuria

• Haematuria

• increased nitrogen (alturia)

• renal casts

• oedema or oliguria (as oedema more marked in nephrotic syndrome)

• anti-streptococcal titres

• hypertension.

..Rx: depends on cause. So does prognosis. If transient or orthostatic it’s benign so leave it. ..Complications of renal disease:

• fluid overload,

• pulmonary oedema,

• intravascular depletion causing acute renal failure,

• loss of complement and other stuff causing infection,

• increased risk of arterial venous thrombosis

• increased risk of cardiovascular disease.

AKI and Acute Tubular Necrosis

Approach to the patient with oliguria:

Aetiology of ARF: rapid decline in eGFR over days to weeks accumulating nitrogenous waste so urea goes up, kidney is unable to filter and produce urine so there is an increase in extracellular volume and a rising of electrolytes especially potassium and you can’t excrete acid so you get acidosis.

These are the emergencies which you need to management acutely.

Aetiology: pre renal, renal and post renal. Pre renal is anything that reduces renal perfusion like hypovolaemia etc; pump failure e.g. after MI; reduced local perfusion; decreased systemic vascular resistance. ACEis and NSAIDs constrict the afferent arterial renal arteries thus reducing renal perfusion. Other antihypertensives might be in toxic doses leading to massive vasodilation.

..Renal causes: immune causes in the glomerulus, IgA nephropathy, immune complex deposition, also systemic like DM and HTN and rare things like lupus etc. Intrinsic renal causes present suddenly unlike pre-renal and post-renal.

• Glomerulonephritis is an umbrella term for an immune-mediated glomerular damage.

• Tubular disease, so the renal tubule which normally reabsorbs so is very metabolically active (first pass at systemic drugs) so goes ischaemic when there is a reduced renal flow. Acute tubular necrosis is ischaemic damage/toxins (NSAIDs, gentamicin, contrast) /pigments such as lead, cadmium, haemoglobin, iron, Wilson’s disease.

• Interstitial disease is the bits between the tubules and is...

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