Renal pathology Flashcards
Discuss renal calculi. (types, formation, consequences)
Calculi form as the result of:
- Supersaturtion -> precipitation into crystals
- Changes in urinary pH -> saturation level reduces with decreasing pH
- Decreased urine volume -> more concentrated urine
- Bacteria -> urea splitting enzymes alkanise the urine making struvite crystal formation more favorable
- Decreased inhibitors of crystal formation, eg pyrophosphate, diphosphonate, citrate, nephrocalcin
Renal calculi result in:
- Ulceration and bleeding
- Obstruction
- Infection
- Pain
- Extravasation
Discuss the causes and pathogenesis of Acute Tubular Necrosis (ATN) (or Acute Kidney Injury (AKI)).
ATN can result from:
- Toxic causes:
- Drugs - aminoglycosides (eg Gentamicin)
- Radiocontrast dye
- Myo/hemoglobin
- Obstruction of blood flow:
- Shock
- Sepsis
- Vessel pathology eg microangiopathies,
- Thrombotic thrombocytopaenia
- DIC
In its early stages ATN is reversible if the causative problem is resolved.
Tubular cells are very sensitive to both ischaemia and toxins.
Injury can be:
- Reversible: Cellular swelling, loss of brush border and polarity, blebbing and detachment, or
- Irreversible: Necrosis and apoptosis.
Damage to tubular cells ->:
- Loss of polarity -> ab(N) ion transport -> inc’d distal Na levels -> vasoconstriction (tubuloglomerular feedback) -> further decline in blood flow -> red’d GFR
- Detachment of injured cells -> casts -> luminal obstruction -> red’d GFR
- Damaged cells allow passage of fluid into the interstitium -> interstitial oedema -> further tubule damage -> red’d GFR
Vasoconstriction also results from:
- stimulation of the renin-angiotensin system (inc’d Na -> tubuloglomerular feedback)
- damage to endolthelial cells ->:
- inc’d release of endothelin,
- dec’d release of NO, and
- dec’d release of prostacyclin
What are the two types of pyelonephritis? Which factors pre-dispose to each type?
Haematogenous:
- debility
- immunosuppression
- septicaemia
Ascending:
- sex
- intrumentation
- vesico-ureteric reflux
- pregnancy(+)
- diabetes
- renal lesions
What are the most common infective agents in pyelonephritis?
Gram –ve bacilli (85%)
- E coli
- Proteus
- Klebsiella
- Enterobacter
- Strep faecalis
- Staph
Outline the glomerular syndromes and include manifestations of each syndrome.
**Nephritic syndrome: **
- haematuria
- azotemia (urea, creatinine)
- variable proteinuria
- oliguria
- oedema
- hypertension
Rapidly progressive glomerularnephritis:
- acute nephritis
- proteinuria
- acute renal failure
Nephrotic syndrome:
- ++ proteinuria (>3.5g/day)
- hypoalbuminuria
- hyperlipidaemia
- lipiduria
Chronic renal failure:
- Azotemia inc’g for months/yrs
Isolated urinary abnormalities:
- Glomerular haematuria +/-
- Sub nephrotic proteinuria
Discuss the immune mechanisms of glomerular injury.
- Antibody mediated
- In situ immune complex deposition
- Circulating immune complex deposition
- Cytotoxic antibodies
- Cell mediated immune injury
- Activation of alternative complement pathway
What renal syndromes are associated with NSAIDs?
- Haemodynamically induced acute renal failure – due to decrease synthesis of vasodilatory prostaglandins
- acute hypersensitivity interstitial nephritis
- acute interstitial nephritis and minimal change disease
- membranous nephropathy
