Vascular, drug-induced and acidiotic nephropathies Flashcards
Treatments for renal artery stenosis
ACEi reduces perfusion to the kidneys because it reduces pressure without increasing flow as it cannot undo the stenosis
Angioplasty and stenting is only beneficial if there is worsening renal failure.
Renal artery stenosis
Can cause malignant hypertension–> high BP and papilloedema
This is atherosclerotic and so has the same RFs as IHD
Fibromuscular dysplasia
Autosomal dominant disorder where the arterial walls undergo normal growth restricting the blood flow and causing stenosis
This affects the kidney and the carotids but does rarely affect the arteries of the abdomen–> treat with ballooning every 2 years
On an angiogram the arteries often look like a string of beads
Drug-induced kidney injury
Can be:
Pre-renal–> hypotension, dehydration or reduced perfusion
Renal–> glomerular injury, interstitial nephritis or tubular
Post renal/obstructive–> Uris acid or other crystal formation
Pre-renal drug-induced nephropathy
In these cases urinary Na is low and urea is much higher than creatinine because the kidney is still working to reabsorb to increase circulating volume || Hypotension–> anti-hypertensive medication || Dehydration–> furosemide/other diuretics || reduced renal perfusion–> ACE inhibitors
Renal drug-induced nephropathy
Glomerular injury–> due to gold or NSAIDs
Interstitial nephritis–> immune mediated so may show allergic symptoms and can come on up to a mon after exposure –> NSAIDs, B-lactams or PPIs
Tubular–> lithium induced diabetes insipidus
Post-renal/obstructive drug-induced nephropathy
Either predispose to crystals of Uric acid (or oxalate) precipitating out and obstructing the collecting ducts–> Orlistat or Allopurinol
This can happen in the renal parenchyma as well
Drugs themselves can precipitate out–> aciclovir, HIV protease inhibitors or methotrexate
Renal tubular acidosis
A metabolic acidosis due to either increased loss of bicarbonate proximally in kidney (over-secretion or poor reabsorption) (type 2) OR Reduced acidification of the urine distally in the kidney (type 1)
Both types have a normal anion gap, if it is raised it is non-renal acidosis
Anion gap
This represents the difference between the total acid and alkali on the body –> (Na+K) - (Cl + HCO3)
Normally it is positive (more acid) up to 12-16mmol/L
Renal tubular acidosis occurs when there is an acidosis with an anion gap of 16 or less
Causes of acidosis with a raised anion gap
This is due to either increased acid ingestion or production:
Ketoacidosis due to –> type 1 DM, starvation or alcohol
Lactic acidosis due to –> sepsis, metaformin or B-adrenoceptor agonists
Methanol or ethylene glycol ingestion (badly made spirits)
Type 1 RTA
Acidosis due to failure to secrete enough acid in the DCT
Due to rheumatoid arthritis or sjorgen’s syndrome, amphotericin B or hypercalciuria
This can be detected by high urine pH, will often get stones or nephrocalcinosis
How would you treat a type 1 RTA
Low dose alkali therapy
Citrate +- bicarbonate
Type 2 renal tubular acidosis
Acidosis due to increased bicarbonate loss, or failure to reabsorb in PCT–> acetozolamide, gammaglobulinaeamia (esp. Myeloma) or hypercalciuria –> general PCT dysfunction Fanconi syndrome
Bicarbonate level ~16mmol/L
May be linked with other PCT dysfunction–> aminoaciduria, glycosuria, phosphaturia
Non-RTA causes of normal anion gap acidosis
Diarrhoea or ureter diversion procedures can cause increased bicarbonate loss
Ureter division can damage the bowel if the urine has high levels of bicarbonate
Treatment of RTA type 2
High dose bicarbonate therapy
This should increased systemic pH correcting the acidosis but will also increase the urinary pH and in case bicarbonate excretion, unlike type 1 RTA treatment
