L11- Tubular and Interstitial Diseases Flashcards
list some examples of tubular and interstitial kidney diseases
- ATN (acute tubular necrosis)
- tubulointerstitial nephritis
- acute polynephritis
- chronic polynephritis
- papillary necrosis
- obstructive nephropathy
- renal stones
ATN is the result of irreversible injury to (1) causing cell death, aka (2), and eventually progresses to (3). The major causes are (4) and (5).
(acute tubular necrosis) 1- renal tubules 2- necrois 3- ARF (acute renal failure- an intrinsic and pre-renal cause) 4- ischemia (more common) 5- toxicity
list the 3 major signs and symptoms of ATN
- acute decline in GFR
- oliguria / anuria
- serum BUN and creatinine increased
list the possible causes of ischemic ATN
- hypotension
- vasodilatory systemic infection (septic shock)
- hemorrhagic shock (GI bleed)
- hypovolemic shock (vomiting, diarrhea)
list the possible causes of Nephrotoxic ATN
Exogenous: i) aminoglycosides, ii) contrast media (CT/cardiac cath)
Endogenous: i) hemoglobinuria, ii) myoglobinuria
Ischemic ATN- has a (diffuse/patchy) necrosis affecting (2) parts of the nephron the most
Nephrotoxic ATN- has (diffuse/patchy) necrosis affecting (4) parts the most
1- patchy: short segments affected
2- straight PCT, ascending LoH
3- diffuse: more extensive
4- PCT
Note- both affect DCT, particularly ascending LoH
describe how toxic and ischemic injury in ATN leads to oliguria/anuria and reduced GFR
Ischemia:
i) vasoconstriction –> dec GFR + tubular injury
ii) tubular injury –> tubular backleak, sloughed cells, interstial inflammation
iii) backleak –> dec urine output / inflammation –> dec GFR / sloughed cells => obstruction –> dec urine and dec GFR
Toxic: skips (i), direct tubular injury
list the 3 clinical phases of ATN
- initiation phase (36 hrs)
- maintenance phase
- recovery phase
in the initiation phase of ATN there is an acute decrease in (1) and a rapid increase in (2)
(1st 36 hrs)
1- GFR
2- serum BUN, creatinine
the maintenance phase of ATN can last for (1), and there is a plateau of (2); key signs and symptoms include (3), therefore (4) may be necessary
(2nd phase) 1- days - 3 wks (oliguria) 2- serum BUN, creatinine 3- uremic Sxs, fluid overload, metabolic acidosis, hyperkalemia (=> arrhythmias / death) 4- dialysis
in the recovery phase of ATN, (1) is restored, leading to an increase in (2) and (3) and a (rapid/gradual) decrease in (5)
(3rd and final phase) 1- tubular function 2- GFR 3- urine output / volume 4- gradual 5- serum BUN, creatinine
list the physical exam findings for ATN Dx
- hypotension
- low urine output = oliguria/anuria
- uremic signs: pericardial friction rub, confusion
list the laboratory (non-urine) findings for ATN
- elevated serum BUN, creatinine
- metabolic acidosis / low HCO3-
- hyperkalemia
- hyperphosphatemia
- anemia (dec EPO - more of a chronic development)
list the urine findings for ATN
- muddy brown granular casts
- epithelial cell casts
- free epithelial cells
- mild proteinuria
- microscopic/mild hematuria
- no pyuria (WBCs/pus)
tubulointerstitial nephritis defines a group of diseases with the following changes to interstitium and glomeruli
- **interstitial inflammation: edema (acute), fibrosis (chronic)
- normal glomeruli
Tubular dysfunction (specifically in tubulointersitial nephritis) will have the following 4 consequences:…
- impaired urinary concentration (polyuria, nocturia)
- salt wasting (hyponatremia)
- metabolic acidosis (dec ability to excrete acid)
- NO significant proteinuria, hematuria
list the acute causes of tubulointerstitial nephritis (TIN)
- drugs (71%), mainly antibiotics
- infections (15%)
- idiopathic (8%)
- sarcoidosis (1%)
list the chronic causes of tubulointerstitial nephritis (TIN)
- infection (pyelonephritis = bacterial; can also be due to viral, parasitic infections)
- analgesic abuse (ASA, acetaminophen)
- urate nephropathy (gout)
list the common drugs that cause tubulointerstitial nephritis (TIN)
(usually acute, but ASA/acetaminophen abuse causes chronic // many are antibiotics***)
- β-lactams (penicillins, cephalosporins)
- sulfonamides (bactrim, furosemide, thiazide diuretics)
- ciprofloxacin
- rifampin
- NSAIDs***
- cimetidine
- allopurinol
- PPIs***: omeprazole, lansoprazole
Drug induced AIN is usually due to a (1) reaction with (2) infiltrating the renal interstitium. It usually appears (3) after starting medication for the first time, or (4) upon second exposure. It will have the following signs and symptoms: (5).
(acute interstitial nephritis) 1- allergic reaction 2- eosinophils, lymphocytes, macrophages 3- 2 weeks 4- 3-5 days 5- (allergic rxn Sxs) fever (27%), rash (15%), eosinophilia (23%), all three (10%) OR ARF / oliguria OR asymptomatic
list the laboratory findings in AIN
(acute interstitial nephritis)
Urine: eosinophils, sterile pyuria, WBC casts, mild proteinuria
Blood: inc BUN, creatinine, eosinophils + hyperkalemia and low HCO3- (via tubular dysfunction)
AIN diagnosis is complete via (1) and treat involves (2) and (3). The prognosis of AIN can be either (4) or (5).
(acute interstitial nephritis) 1- renal biopsy 2- stop drug 3- oral steroids to aid recovery 4- complete recovery 5- incomplete (40%): persistent creatinine elevation
in acute pyelonephritis, the affecting microbes enter the kidney through either (1) or (2) [indicate which is more common]
1- bloodstream: seeding from distant source, i.e. bacterial endocarditis, septicemia
2- (more common) ascending infection: from lower urinary tract (bladder, ureter)
in acute pyelonephrits where the initial infection starts in the bladder:
- women bacterial sources are (1)
- men bacterial sources are (2)
1- bacterial colonization of introitus (vaginal opening) and distal urethra –> bladder due to short urethra and can stem from Foley’s cath. or sexual intercourse
2- entry into bladder (with bacterial colonization) due to BPH (obstruction), catheterization, urine stasis, retrograde travel up to ureters then kidneys (vesicoureteral reflux- more in chlidren)
