Pathoma 12.1 Congenital Kidney Disease, 12.2 Acute Renal Failure
Terms in this set (55)
Congenital kidney disease (5)
1. horse shoe kidney
2. renal agenesis
causes cyst formation
3. dysplastic kidney
4. polycystic kidney disease (PKD)
5. medullary cystic kidney disease
what is the most common congenital renal anomaly? What does it look like?
- conjoined kidneys connected at lower pole
where is horseshoe kidney usu. found? why?
- kidney starts in the pelvis and ascends to abdomen normally, but now it is stuck under inferior mesenteric a.
2 types of renal agenesis
complication of unilateral renal agenesis
1. pt lacks 1 kidney
2. hypertrophy of existing kidney
3. hyperfiltration increases risk of renal failure later in life
what causes bilateral renal agenesis
(USMLE) what syndrome oligohydraminos cause? what symptoms does it include (3)? what is its outcome
Potter sequence - incompatible w/ life
1. lung hypoplasia
2. flat face + low set ears
3. developmental defects of ext.
What is dysplastic kidney?
noninherited, congenital malformation of renal parenchyma w/ cysts + abnormal tissue esp. cartilage
What is genetic transmission of dysplastic kidney?
What does dysplastic kidney look like histologically?
Cystic space + tissue + cartilage
Is dysplastic kidney usually unilateral or bilateral?
usually unilateral, but bilateral on exams to try to confuse you into thinking PKD
What is Polycystic Kidney Disease?
bilateral enlarged kidneys filled with cysts in cortex and medulla
(USMLE) who gets autosomal recessive PKD? what is it associated with (2)? what does the newborn also presents with?
1. congenital liver hepatic fibrosis & cysts
2. baby with portal HTN & renal failure
- newborns may present w/ Potter sequence (so bad it is as if he has no kidney)
who gets autosomal dominant PKD? what symptom is it associated with (CV-1, urine, kidney)?
affect young adults
3. worsening renal failure (causing high plasma renin)
what gene mutation causes autosomal PKD?
APKD1 or APKD2
cysts start developing at birth, symptoms shows up over time
what 3 disease is autosomal dominant PKD associated w/?
1. berry aneurysm -
2. liver cysts
3. mitral valve prolapse
(if the stem has renal disease & brain hemorrhage causing death, think autosomal dominant PKD; think cyst in liver, cysts in brain, cysts in kidney)
what type of inheritance is medullary cystic kidney disease
where does the cyst grow in medullary cystic kidney disease?
cysts in medullary collecting ducts
How can you differentiate medullary cystic kidney disease from PKD? how will the pt present?
Shrunken kidneys (as opposed to enlarged in PK)
pt will have worsening renal failure
what is the hallmark of renal failure? how is it quantified? what does it usu. cause?
azotemia i.e. increased nitrogenous waste in the blood
- measured by increased BUN & creatinine
- pt oft has oliguria
3 causes of azotemia (urine production)?
Pre-renal azotemia: decreased blood flow
Post-renal azotemia: blockage of outflow
pre-renal azotemia: GFR & urine level
1. Decreased blood flow & therefore GFR
physiology of normal serum BUN, Creatinine & their ratio
1. BUN & creatinine are both filtered by the glomerulus
2. some BUN will return to the blood, but creatinine cannot be reabsorbed
3. in normal kidney, BUN to creatinine ratio is 15
(USMLE) Why is serum BUN:Creatinine ratio > 15 in pre-renal azotemia?
1. pre-renal blockage
2. RAA activated, aldosterone up, Na+ reabsorbed, also water, BUN follows
3. both creatinine and BUN rise but BUN more b/c BUN not filtered AND reabsorbed way more
Why is FENa < 1% in pre-renal azotemia? what will be the urine osmolality be?
so they can reabsorb Na+, concentrate urine
urine osmolality will be >500 (very concentrated urine)
(FENa = fractional reabsorption of Na+)
Why do you get decreased GFR, azotemia and oliguria in post-renal azotemia?
blockage leads to back pressure into glomerulus, decreased GFR, azotemia, oliguria
Why is BUN:Cr > 15 in early stages?
increased tubular back pressures "forces" BUN back into blood
Why is FENa < 1% in post-renal azotemia? what is the urine osmolality
Tubules intact, can reabsorb Na+, concentrate urine
urine osmolality >500
(FENa = fractional excretion of Na+)
What happens in long standing post-renal obstruction?
serum BUN:Cr < 15
Tubules damaged, can't reabsorb BUN
What is FENa in long standing post-renal obstruction? what about urine osmolality?
FENa > 2%
Tubules damaged can't reabsorb Na+, can't concentrate urine (urine osm < 500)
What is most common cause of intra-renal azotemia (and acute renal failure)?
Acute Tubular Necrosis
injury/necrosis of tubular epithelial cells
Why do you get decreased GFR in ATN?
necrotic cells plug tubules, obstruction decreases GFR
Why is BUN:Cr, FENa, urine osmolality in ATN?
serum BUN:Cr < 15: Tubules damaged, can't reabsorb BUN
FENa >2%: decreased reabsorption of Na+
urine osmolality <500: cannot concentrate urine
What do you see in urine in ATN?
Brown, granular casts (dead tubular cells sloughed off; it's a cast b/c it is casted in the shape of the tubule)
Histology for ATN
3 T's (right) =
1. epithelial cell necrosis (no nuclei) & detached from basement membrane (better seen on the right edge of the top tubule)
2. necrotic cells filling lumen forming granular cast
1 T (left) = normal, alive tubule, patent, epithelial cells have nuclei & attach to BM
What are 2 most common causes of ATN?
What is common cause of ischemic ATN?
long-standing pre-renal azotemia causing decreased blood flow
(kidney really needs the blood supply b/c it does a lot of work)
What two parts of kidney are particularly susceptible to ischemic ATN?
1) Proximal tubule
2) Medullary segment of thick ascending limb of Loop of Henle
(doing most work)
What causes nephrotoxic ATN? what part of the kidney is more susceptible
toxic agents cause necrosis
proximal tubule is more susceptible
What toxic agents typically cause ATN (6)?
(2- environmental, 2 treatment related, 2- from body)
1. Aminoglycosides (antibiotic) + (uw) amphotericin B
2. Heavy Metals (e.g. lead)
3. Myoglobinuria (e.g. crush injury)
4. Ethylene Glycol (antifreeze)
5. Radiocontrast dye
(USMLE) Child drinks antifreeze (ethylene glycol), what type of crystals form in urine?
(mnemonic: ethylene gly"CO"l = calcium oxalate (crystal has x in it)
classic example of urate nephropathy; how is it prevented
tumor lysis syndrome
1. in chemotherapy e.g. leukemia, drug kills a large amt. of cell in the blood
2. rapid cell death release nuclear material causing uric acid build up
3. uric acid damage tubule
prevented by hydrating pt prior to rx; or allopurinol to prevent uric acid build up
3 clinical features of ATN (urine, serum level, acid/base)
1. oliguria w/ brown, granular cast
2. elevated BUN & creatinine
3. hyperkalemia w/ metabolic acidosis
What causes hyperkalemia in ATN? what causes the metabolic acidosis? what type of acidosis is it?
hyperkalemia: decreased K+ excretion (tubular cells need to regrow)
metabolic acidosis: cannot excrete metabolic acids w/ increased anion gap
Is ATN reversible
yes, tubular cells an regenerate;
but needs dialysis b/c electrolyte imbalance can be fatal
How long can oliguria persist even after treatment?
2-3 weeks (tubular cells are stable cells; take time to reenter cell cycle and regenerate)
What is 3rd cause of ATN?
Acute interstitial nephritis (usu. drug induced)
3 drugs that can cause Acute Interstitial Nephritis
Acute Interstitial Nephritis histology
inflammatory infiltrate in the connective tissue between (healthy) tubules
How does Acute Interstitial Nephritis present? (urine vol, pt s/s - 2)
1. low urine
3. rash days to weeks after starting drug
(USLME) What is dead-giveaway in urine for Acute Interstitial Nephritis?
Eosinophils in urine
How to fix acute interstitial nephritis
stop the drug
What can is feared complication of Acute Interstitial Nephritis
renal papillary necrosis
Renal Papillary Necrosis symptoms (urine, what pn)
5 conditions are associated with Renal Papillary Necrosis? (mnemonic)
Analgesics (chronic abuse e.g. analgesic, phenacetin)
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