HLK Week 5 Flashcards
What % of renal plasma flow filters into Bowman’s capsule? How much of that flows back into the peritubular capillaries?
- About 20%
- 99%
What is the composition of the filtrate in Bowman’s capsule?
Basically just like plasma, except virtually no protein.
In addition to the foot process and slit membrane, what ultimately prevents protein from being filtered in Bowman’s capsule?
There’s an electrical barrier of negative charge in Bowman’s space that prevents proteins from filtering.
How is inulin used to measure GFR?
- Freely filterable across glomerular capillaries
- Not reabsorbed in tubules
- Not secreted
- Therefore, amount excreted is equal to amount filtered.
Does creatinine over- or underestimate the true GFR?
Overestimates it because a little is secreted by tubules.
When the clearance of a substance is less than the GFR, it is…?
Reabsorbed.
2 things that are needed to make a concentrated urine:
- Loop of Henle
- Vasopressin
What 2 mechanisms downregulate the release of vasopressin? Which is more sensitive?
- Low osmolality
- High ECF volume
- Osmolality is more sensitive
True or false: measuring plasma sodium is the best way to measure sodium balance.
False: plasma sodium is an indicator of water balance, not sodium balance. So, measuring plasma Na is not a good way to test for hyponatremia.
Explain how the macula densa affects renin secretion:
Osmoreceptors in the macula densa sense salt in the ascending limb of the loop of henle and downregulate renin secretion.
What is the most common INTRINSIC cause of acute kidney injury?
Acute tubular necrosis
True or false: BUN rises out of proportion with creatinine in pre-renal states.
True
How do acidosis/alkalosis affect movement of potassium into/out of cells?
What’s the easy way to remember this?
- Acidosis = movement out of cells = hyperkalemia
- Alkalosis = movement into cells = hypokalemia
- If “ka” is in the word, Ka is in the cell. Al-ka-losis = Ka moves in
What type of imaging is needed to diagnose minimal change disease?
Electron microscopy
What is the preferred treatment for minimal change disease?
Prednisone + ACE inhibitor
Lab finding that is very specific for glomerular disease:
Acanthocytes or RBC casts
Describe the pathophysiology of minimal change disease:
Destruction of podocytes leads to proteinuria, which changes the oncotic pressure in systemic capillaries, causing edema.
Nephritic vs. Nephrotic
Nephritic: inflammatory infiltrate - Hematuria - Decreased GFR leads to oliguria, HTN Nephrotic: massive proteinuria - Hypoalbuminemia - Loss of oncotic pressure leads to edema
Is it necessary to do a biopsy in kids with proteinuria?
Not unless they don’t respond to steroids. 90% of proteinuria in kids is due to minimal change disease, so it’s assumed to be this unless they don’t respond to Tx.
Very common cause of glomerulonephropathy, especially in Asia:
IgA Nephropathy (aka Berger’s disease, or Henoch-Schonlein purpura if systemic)
How do adrenergic agonists lead to hypokalemia?
- (Nor)epinephrine and other adrenergic agonists increase activity of Na-Ka-ATPase, which moves Ka into cells.
- The corollary is that B-blockers cause hyperkalemia.
How does insulin lead to Ka uptake by cells?
- Also stimulates activity of Na-Ka-ATPase.
- The corollary is that diabetes can cause hyperkalemia.
Explain how aldosterone regulates Ka levels:
Acts on the distal tubule to excrete Ka in exchange for reabsorption of Na into the body.
How does urine flow rate contribute to hyper/hypokalemia?
- Increased urine flow rate = increased Ka excretion, leading to hypokalemia.
- Decreased rate = decreased Ka excretion, leading to hyperkalemia.
Why is it bad to use NSAIDS with ACE’s/ARB’s
ACE’s/ARB’s dilate efferent arteriole and NSAID’s constrict afferent arterioles. Together, this dramatically reduces GFR.
Treatment of acute hyperkalemia:
- Get ECG if Ka greater than 5.9
- Stabilize myocardium if ECG is abnormal
- Increase cellular uptake of Ka: insulin
- Increase excretion of Ka: kayexalate (GI), loop diuretic, dialysis.
How can you tell if hypokalemia is due to kidney dysfunction or GI dysfunction?
- If GI, urine Ka will be appropriately conserved (i.e., low).
- If kidney, urine Ka will be high
What is the hallmark sign of hypokalemia on ECG?
Appearance of U wave
How does alkalosis affect plasma CA?
- Alkalosis = increased CA binding to albumin
- Total CA levels unchanged
What is the first step in a patient with hyponatremia?
Measure plasma osmolality to determine whether the hyponatremia is hyposmolar, isosmolar of hyperosmolar.
When do you have to worry about the risk of Central Pontine Myelinolysis?
Hyposmotic hyponatremia
SIADH:
- ADH is made without appropriate stimulus
- Plasma osmolality is low
- Euvolemic
- Enhanced ADH action in kidney (UOsm > POsm)
What are the challenges to measuring CrCl with 24 hour urine collection?
- Incomplete collection
- Day to day variation
- Must be in a steady state
Indications for dialysis:
A- Acidosis E- Electrolyte imbalance I- Ingestions O- Volume overload U- Uremia
Which aminoglycoside is the least nephrotoxic?
Streptomycin
Drugs that can cause acute tubular necrosis (ATN):
- Antibiotics: aminoglycosides, amphotericin B, vancomycin, cephalosporins
- Acyclovir
- Cyclosporine
- Antineoplastics such as cisplatin
Interpret the finding of a red/brown supernatant that’s positive for heme:
Probably myoglobinuria due to rhabdomyolysis, which can lead to acute tubular necrosis.
Drugs that can cause interstitial nephritis:
- PCN’s/cephalosporins/sulfonamides
- Sulfonamide-containing diuretics
- NSAIDS
- Rifampin, phenytoin, allopurinol
- PPI’s
Mnemonic for drugs that can cause acute tubular necrosis (ATN):
ATN:
- Antibiotics/antivirals/ACE’s (aminoglycosides, amphotericin B, vancomycin, cephalosporins, acyclovir)
- Transplant drugs (cyclosporine)
- Neoplastic drugs (cisplatin)
Treatment for interstitial nephritis:
- Removal of offending agent (drug, if drug induced)
- Steroids sometimes helpful
Essentials of Dx of acute interstitial nephritis:
- Fever
- Arthralgia
- Rash
- White cell casts, hematuria, sterile pyuria
Common lab findings in acute tubular necrosis:
- Hyperkalemia
- Hyperphosphatemia
- Muddy brown casts in urinalysis
- BUN/creatinine ratio less than 20:1
Essentials of Dx of acute tubular necrosis:
- Acute kidney injury
- Ischemic or toxic insult or sepsis
- Nephrotoxins (drugs and dyes)
- Urine sediment with muddy brown casts and tubular epithelial cells
Essentials of Dx of acute glomerulonephritis:
- Acute kidney injury
- Hematuria, proteinuria, dysmorphic red cells and red cell casts
- Dependent edema (esp periorbital, scrotal) and HTN
Anti-GBM antibodies are associated with which disease?
Goodpasture syndrome
What causes injury in Goodpasture syndrome?
Autoantibodies against basement membrane type IV collagen.
Some common causes of acute glomerulonephritis due to immune complex deposition:
- Lupus
- IgA nephropathy (Berger’s disease)
- Endocarditis
- Post-infectious glomerulonephritis
- Cryoglobulinemic glomerulonephritis (seen with Hep C)
True or false: acute glomerulonephritis is a common cause of acute kidney injury.
False: only about 5% of acute kidney injuries are due to glomerulonephritis.
Pauci-immune acute glomerulonephritis:
- Includes granulomatosis with polyangitis (Wegener’s dz) and microscopic polyangitis.
- Immune-cell mediated tissue damage
- Can evolve to crescentic glomerulonephritis with poor prognosis unless treatment is started early.
True or false: elevated BUN and creatinine cannot be used to distinguish acute kidney injury from CKD.
True
Common etiology for rapidly progressing glomerulonephritis (RPGM):
Any of the immunologic conditions:
- Anti-GBM
- ANCA diseases
- Immune complex deposition diseases
SSx of uremia:
- Asterixis
- Pericardial rub
- Altered mental status
- Seizures
Urine pattern seen in post-renal disease:
Bland sediment
Urine pattern seen in pre-renal disease:
- Concentrated urine
- Hyaline casts
Urine pattern seen in ATN:
- Renal tubular epithelial cells
- granular casts
- “muddy brown casts”
Essentials of renal artery stenosis:
- Can be caused by atherosclerosis or fibromuscular dysplasia (less common)
- HTN
- ACE’s cause acute kidney injury
