Nephrology Flashcards
What is the treatment for SBP in PD patients
Intraperitoneal antibiotics preferred unless systemically septic
Gram +ve cover and anaerobs
- VANCOMYCIN
- CEFUROXIME+ GENT
Sepsis:
Tazocin
Ciprofloxacin - watch out for photosensitive rash as SE
What is nephrogenic systemic fibrosis
Defintion:
Systemic fibrosis of skin
-cuteanous demopathy seen in ESRF
-aetiology unknown
Triggers:
Gadolinium based contrast agent
metformin
presentation: worsening skin tightetning with joint contractures inpulling of umbilicus cutaeneous dermopathy = WOOD LIKE SKIN pulmonary fibrosis + pulm htn cardiomyopathy due to fibrosis
How does renal cell carcinoma present?
Unilateral Renal mass hydrocoele may be present if ocmpression or invasion of testicular vein occurs metastases haematuria renal flank mass loin pain
Mx:
Nephrectomy
small kinase inhibitors - Anti VEGF
-once primary removed - secondaries do tend to regress
portion of renal cell is bilateral - cannot perform nephrectomy in this case
no place for chemo radiotherapy
Familial mediterranean fever
Abdominal pain - recurrent without cause
fever periodically
arthritis
nephrotic syndrome
Nephrotic syndrome is caused by Renal Amyloidosis
25% pericarditis and pleuritis
mediterranean and jewish descent
Mx:
Colchicine delays renal CKD
Renal transplant
How does RTA 1 present - What is the defect?
CLASSIC RTA
DCT
Defect:
Failure to excrete H+ and reabsorb K+ at DCT exchanger
retain H+ - no urine acidification so can cause stones
no K reabsoprtion from passive diffusion back into lumen from LoH
Alakline urine
hypokalaemia
metabolic acidosis
renal stones - predisposition to stone formation in alkaline environment
How is RTA 2 managed -how does it present?
PCT
Often associated with FANCONI SYNDROME = PCT absorption dysfunction
Failure to reasorb HCO3
Hypokalaemic metabolic acidosis
urinary alkalinisation typically
H+ excretion defect as well therefore K+ preferentially excreted to acidify urine and correct acidosis
Typically multiple other PCT defects go along with it
How is RTA 4 managed -how does it present?
Actually an effect of hypoaldosteronism and nothing to do with RTA 1/2
Effect of lowered excretion of ammonia
Hypoaldosteronism = hyperkalaemia and Hyponatraemia
and hypotension
normal anion gap still
What is renal tubular acidosis
Failure of the renal tubules to maintain Acid base balance leading to a metabolic acidosis
type dependent on RTA type
RTA 1 = DCT K+/H+ exchanger
HYPOKALAEMIC MET ACIDOSIS
NORMAL ANION GAP
RTA 2 = PCT usually in assoc with FANCONI multiple reabsorption defects hypokal met acidosis as RTA 1 add hypomag / hypocal / hypophos
RTA 4
Adrenal issue - secondary to hporeninemic hypoaldosteronism
i.e. hyperkalaemia and hyponatraemia
What is Bartters syndrome?
Congenital defect in Thick Ascending limb of LoH
Defect Na/K/2Cl channel - SALT WASTING
Hypotension
Metabolic alkalosis (H+ excretion to reabsorb K+)
Hypokalaemia
EARLY PRESENTATION
Hypotension - lose salt concentration gradient medulla - water losing therapy also association with Mag loss / Cal loss
No reabsorption Na
No net movement water
No net movement of charge - no mag absorption
K+ remains in lumen
Compensatory exchange to sequester lost K+
What is Gitelman syndrome
Congenital defect in Thiazide NaCl cotransporter channel in DCT
As defect is fairly small compared to barters patients are often asymptomatic
Hypokalaemia hypomagnesic metabolic alkalosis
The Na/K basolateral antiporter continues to function
Net movement of K+ from blood into luminal cell
K+ exchanged for Calcium and is lost.
Attempt to reabsorb K+ via H+ antiporter = alkalosis
Lack of net movement of Positive charge limits Magneisum absorption
What does liquorice intoxication cause?
liquorice increase enzymatic conversion of cortisol to cortisone which has crossover mineralicorticoid activity
This results in hyperaldosteronism without adlosterone
low renin low aldosterone HTN low K+ - excreted in excess hypernatraemia
Whats is SAME syndrome?
Syndrome of apparent mineralicorticoid excess
Overactive conversion of cortisol to cortisone - genetic
11BHSD2 gene
low renin low aldosterone HTN low K+ - excreted in excess hypernatraemia
What condition is associated with renal failure in Caribbean descent?
Renal artery fibromuscular dysplasia
- Hypertension - treatment resistant due to hyperreninaemic hyperaldosteronism
- CKD
How is membranous nephropathy treated?
Treatment:
Marked proteinurea
HTN
deteriorating renal function
prednisolone
cyclophosphamide
88% remission at 10 years follow-up
Rituximab may be used for steroid resistant disease
What is membranous glomerulopathy associated with
2nd most common cause of nephrotic syndrome
steroid responsive
Also most commonly associated with chronic NSAID use
