Chapter 12 Flashcards
A Horseshoe kidney would get snuck on what structure?
IMA
What is renal agenesis?
Absent kidney formation (may be unilateral or bilateral) usually lading to hypertophy of the existing kidney
What does bilateral renal agenesis lead to?
Potter sequence- with oligohydramnios with lung hypoplasia, flat face with low set ears, and developmental defects of the extremities
Describe a dysplastic kidney
Noninherited, congenital malformation of the renal parenchyma marked by cysts and abnormal tissues
Note that this is usually unilateral but must be dsitignuished from inherited polycystic kidney disease if bilateral
What is this?
Polycystic kidney disease- an inherited defect leading to bilateral enlarged kidnyes with cysts in the renal cortex and medulla
How does the AR form of PKD present?
Presents in infants as worsening renal failure and HTN or with Potter sequence in newborns
How does the AD form of PKD present?
Presents in young adults as HTN due to increasd renin, hematuria. and worsening renal failure
The main associations of PKD are:
Berry aneurysm, hepatic cysts, and mitral valve prolapse
What is medullary cystic kidney disease?
AD inherited defect leading to cysts in the medullary collecting ducts resulting in parenchymal FIBROSIS leading to shrunken kidneys and renal failure
What is the hallmark of acute renal failure?
Acute, severe decrease in renal function developing within days with a hallmark of azotemia (increased BUN and Cr), often with oliguria
Divided into prerenal, postrenal, and intrarenal based on etiology
What are the main causes of prerenal azotemia?
Due to decreased blood flo to the kidneys (e.g. cardiac failure, renal steneosis) resulting in decreased GFR< azotemia, and oliguria
What are the main lab findings of prerenal azotemia?
Reabsorption of fluid and BUN ensues (serum BUN:Cr > 15);
tubular function remains intact (fractional excretion of sodium (FENa) < 1%)
and urine osmolarity remains > 500 mOsm/kg
What are the main causes of postrenal azotemia?
Due to obstruction of the urinary tract downstream from the kidney resulting in decreased outflow and subsequent decreased in GFR with onset of azotemia and oliguria
What are the main lab findings of postrenal azotemia?
During early stages of obstruction, increased tubular pressure forces BUN into the blood (serum BUN:Cr >15), FENa remains <1%, and urine osm >500 BUT
with long-standing: serum BUN:Cr <15, FENa >2%, and urine osm <500mOsm/kg
What is acute tubular necrosis?
Injury and necrosis of the tubular epithelial cells (most common cause of acute renal failure; intrarenal azotemia)
What are the urinaylsis findings of acute tubular necrosis?
Brown, granular casts (necrotic cells lug the tubules and GFR decreases)
serum BUN:Cr <15, FENa >2%, and urine osm < 500
What are the main etiologies of acute tubular necrosis?
Etiology may be iscehmic (derceased blood supply resuts in tubular necrosis) or nephrotoxic (toxic agents induce necrosis)
Ischemia- often preceded by prerenal azotemia and the proximal tubule and medullary sgemnt of the thick ascending limb are particularly susceptible to ischemic injury
Describe nephrotoxic damage to the kidneys
- Proximal tubules is most susceptible
- Amingoglycosides, heavy metals, myoglobinuri (from muscle injury), ethylene glycol, urate (TLS)
________ are used prior to chemo to decrease the risk fo urate-induced ATN
Allopurinol (and hydration)
Clinical features of ATN
Oliguria with brown, granular casts
Elevated BUN and Cr
Hyperkalemia due to decreased renal excretion with metabolic acidosis
What is acute interstitial nephritis?
Drug induced hypersensitivity involving the interstitium and tubules resulting in acute renal failure (intrarenal)
causes include NSAIDS, penicillin, and diuretics
How does acute interstitial nephritis present?
oliguira, fever, and rash days-wekeks after starting a drug; eosinophils may be seen in urine
Resolves with drug cessation but may progress to renal papillary necrosis
What are the main causes of renal papillary necrosis?
Sickle cell
Severe acute pyelonephritis
Diabetes mellitus
Analgesic abuse
What is the basis of nephrotic syndrome?
Glomerulus dysfunction marked by proteinuria (3.5+g/day) resulting in:
Hypoalbuminemia- pitting edema
Hypogammaglobulinemia- infection risk
Hypercoaguable state due to loss of antitihrombin III
Hyperlipidemia and hypercholesterolemia- may result in fatty casts in urine
What is the most common cause of nephrotic syndrome in children?
Minimal Change Disease
What causes Minimal Change Disease?
Usually idiopathic but may be associated with Hodgkin lymphoma
How does MCD appear on imaging?
H&E- normal glomeruli with normal BM
Effacement of foot processes on EM
Negative immunoflourescence (no immune complex deposition)