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81 Cards in this Set
- Front
- Back
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Charge barrier of glomerulus
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heparan sulfate
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clearance equation
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(urine conc x urine flow rate)/plasma concentration
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C = GFR
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no net excretion or reabsorbtion
- inulin ~ creatinine |
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glucosuria at what level
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160-200 mg of glucose
- at 350 mg all transporters are full |
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How does PTH lower phosphate level?
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inhibits Na+/phosphate cotransporter in proximal tubule
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ATII effect on proximal tubule
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stimulates Na+/H+ exchange
--> Na+ and H20 reabsorbed --> contraction alkalosis |
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NSAIDS and renal failure
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Inhibit prostaglandin formation --> decreased dilation of afferent arterial --> decreased GFR
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Beta agonist effect on K
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shifts into cells
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hypo-osmolality on K
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shifts into cells
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digitalis on K
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blocks Na+/K+ ATPase --> shift K out of cells
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Winter's formula
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- for PCO2 compensation
1.5 (bicarb) +8 +/- 2 - 0.7 increase in PCO2 for every 1 bicarb |
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anion gap acidosis
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MUDPILES
Methanol Uremia Diabetic ketoacidosis Paraldehyde or phenformin Iron, INH Lactate Ethylene Glycol Salicylates |
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normal anion gap metabolic acidosis
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Diarrhea
Glue sniffing Renal Tubular acidosis Hyperchloremia |
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Type 1 renal tubular acidosis
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Distal
- H+ ATPase in alpha intercalated cell of collecting tubule impaired - More K+ into urine to balance charge --> increase pH --> increased calcium containing stones - hypokalemia |
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Type 2 RTA
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proximal
- defect in bicarb reabsorption - hypokalemia, hypophosphatemic rickets |
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Type 4 RTA
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hyperkalemic
- hypoaldo or lack of response to aldo - hyperkalemia - less ammonia excretion in proximal tubule --> decreased urine pH --> decreased buffering capacity |
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RBC casts
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glomerulonephritis
ischemia malignant hypertension |
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WBC cast
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tubulointerstitial inflammation
Acute pyelonephritis transplant rejection |
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Granular cast
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"muddy brown"
- ATN |
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Waxy cast
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Advanced renal disease/CRF
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RBCs, no casts
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bladder cancer or kidney stones
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WBCs, no casts
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Acute cystitis
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spike and dome appearance
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Membranous glomerulonephritis (diffuse membranous glomerulopathy)
LM- GBM thickening, diffuse capillary EM- spike and dome SLE, drugs, infections *most common cause of adult nephrotic syndrome |
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Thickened GBM + mesangial expansion
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Diabetic glomerulonephropathy
- NEG of GBM --> increased permeability and thickening - NEG of arterioles --> increased GFR --> mesangial expansion *nodular glomerulosclerosis |
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Focal Segmental Glomerulosclerosis
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Nephrotic
- LM- segmental sclerosis, hyalinosis - HIV patients |
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MPGN pathogenesis
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subendo ICs
Type I- tram track- split GBM - HBV/HcV Type II- dense deposits on EM - C3 nephritic factor |
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Nephritic syndrome
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Inflammatory
- glomeruli involvement - hematuria- RBC casts - azotemia (high nitrogen in urine) - oliguria - hypertension - proteinuria (less than 3.5g/day) |
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subepi immune complexes
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ICs in poststrep
- Type III hypersensitivity- ICs in blood |
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rapidly progressing glomerulonephritis
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nephritic
- crescentic- fibrin, plasma proteins, parietal cells, monos, macrophages - poor prognosis 1. Goodpasture- type II hypersensitivity 2. Wegener's 3. Microscopic polyarteritis (p-ANCA)-no immune complexes |
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Diffuse proliferative glomerulonepthritis
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Nephritic
- subendo DNA-anti-DNA ICs --> wire looping of capillaries *most common cause of death in SLE |
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ICs in mesangium
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Berger's- IgA glomerulopathy
- increased IgA - present with or flares with URI or acute gastroenteritis |
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Alport syndrome
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mutation in type IV collagen- split basement membrane
- ocular, deafness, nerve disorder X linked |
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NSAID nephropathy
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1. chronic interstitial necrosis
2. papillary necrosis * can progress to tubular atrophy |
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large eosinophilic glassy casts can be...
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MM!
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Lithium's effect on kidney
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antagonizes ADH downstream effects
- Lithium binds another receptor - nephrogenic diabetes insipidous |
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Risk in recovery phase of ATN
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hypokalemia from polyurea
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most common kidney stones
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calcium oxalate
- cancer, PTH, vit D, milk-alkali, ethylene glycol, vit C |
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Kidney stones from urease positive bugs
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2nd most common
Ammonium magnesium phosphate (struvite) - proteus, staph, klebsiella - staghorn calculi |
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hexagonal stones
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cystine
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polygonal clear cells in renal tubule cells
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renal cell carcinoma
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Transitional cell carcinoma- bladder associations
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Pee SAC
Phenacetin- analgesic Smoking Aniline dyes Cyclophosphamide |
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histologic changes in ATN
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loss of cell polarity
epithelial detachment necrosis granula "muddy brown casts" |
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"muddy brown casts"
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ATN
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Sickle cell and kidney injury
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Acute papillary necrosis
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Tx for chronic calcium stones
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Thiazide
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left sided varicocele?
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left renal vien thrombosis
- ATIII loss in urine from nephrotic syndrome --> thrombus |
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PAH used to estimate...
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RPF
- absorbed and secreted (proximal tubule) |
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renal angiomyolipoma
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tuberous sclerosis
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liver cysts + bilateral renal tumors + cerebellar hemangiomas
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VHL
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ash leaf spots
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tuberous sclerosis
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clear part of "clear cells"
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glycogen and lipid that was dissolved in preparations
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Ethacrynic acid
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same as furosemide
* not a sulfonamide |
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triamterene and amiloride
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blocks Na channels of CCT
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Subendo ICs
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1. DFGN (nephritic)
- DNAanti-DNA ICs 2. MPGN - tram track or dense deposits |
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Fanconi's syndrome
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decrease proximal tubule transport
Causes: Wilson's, glycogen storage diseases, drugs (cisplatin, expired tetracycline) |
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Potter's in utero is a sign of what kidney disease?
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ARPKD- autosomal recessive (unlike ADPKD)
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Respiratory complications with potter's?
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amniotic fluid in lungs --> immature lungs
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Cysts from dialysis are in what region
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cortical and medullary
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Tx for quadriplegics with urinary incontinence
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antimuscarinic- decreases parasympathetic voiding reflex
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sulfa kidney drugs
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1. Acetazolamide
2. Furosemide 3. Hydrocholorothiazide |
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kidney drugs that can be used in gout
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Ethacrynic acid
NOT furosemide or hydrochlorothiazide |
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thiazide side effects
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Hyper GLUC
- glucose - lipids - Urea - Calcium |
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loop diuretic side effects
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OH DANG
Ototoxicity Hypokalemia Dehydration Allergy (sulfa) Nephritis (interstitial) Gout |
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diuretics that cause acidemia
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1. acetozolamide
2. Spironolactone etc 3. |
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diuretics that cause alkalemia
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loop, thiazides
1. contraction alkalosis from increased ATII (increased Na+/H+) exchanger 2. decreased K --> K leaving cells, H+ going in 3. In low K, H+ leaves in cortical collecting duct |
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ACE i side effects
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CAPTOPRIL
Cough Angioedema Proteinuria Taste changes hypOtension Pregnancy problems (fetal renal damage) Rash Increased renin Lower angiotensin II Hyperkalemia * Don't use in bilateral renal stenosis --> b/c significant decrease in GFR |
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vomiting causes what acid/base disturbance?
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metabolic alkalosis- Loss of gastric secretions
* Mallory weiss tear |
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calcineurin downstream effect
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dephosphorylates NFAT --> NFAT enters nucleus --> IL-2 promoter genes turned on
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Amphothericin B effect on kidney
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1. Decreased GFR
2. Direct toxicity to distal tubule --> increased permeability --> hypokalemia, hypomagnesemia - premature beats etc |
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which region of the collecting duct does ADH work on
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medullary
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Where does ATN effect first
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proximal tubule and 1st part of descending limb- in outer part of medulla
- Also use ATP- so first to be affected |
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bevacizumab
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Anti VEGF antibody
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medullary sponge kidney
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benign, congenital
- cystic dilations of medullary collecting ducts - can develop STONES, hematuria, UTI |
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concentrations don't change in proximal tubule
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Na, K
- reabsorbed with water |
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renal cell carcinomas come from which cells in kidney
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proximal tubule
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why is mostly albumin lost in Minimal change disease
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-loss of polyanions in GBM --> no repulsion with albumin --> allowed to cross
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what can prevent the progression diabetic nephropathy?
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ACE and ARB inhibitors
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No tubular reabsorption or secretion
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Inulin
mannitol |
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Net tubular secretion
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PAH, creatinine
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positive leukocyte esterase and negative nitrite test for UTI. which bug?
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- bacteria
- Entercoccus faecalis |
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E.coli uropathogenic have what
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p-pilli to adhere
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