Renal Random Facts Flashcards
What does the mesonephros become?
Men- Wolffian ducts (ductus deferens and epidydimus); Women- vestigal Gartner’s duct
What is a multi cystic dysplastic kidney
Due to abnormal interaction between ureteric bud and metanephric mesenchyme. Leads to a nonfunctional kidney consisting of cysts and connective tissue
Relationship to ureter to ductus deferens
Ureters pass under the ductus deferens
What do the uterine vessels travel in?
Cardinal ligament
What is the 60-40-20 rule?
60% total body water: 40% intracellular, 20% ECF
How do you measure plasma volume and extracellular volume?
Plasma volume measured by radio labeled albumin, extracellular volume measured by inulin
Equation for renal blood flow
RBF=RPF/(1-Hct); RPF is the clearance of PAH
How does changing the plasma protein concentration change the GFR, RPF, and FF?
Increased plasma protein concentration decreases the GFR, doesn’t affect the RPF, and therefore decreases the FF (GFR/RPF)
Hartnup disease
Autosomal recessive, deficiency of neutral amino acid transporters in proximal renal tubular cells and on enterocytes, causes a neutral aminoaciduria and decreased absorption from the gut
What is Fanconi syndrome
Generalized reabsorptive defect in PCT, associated with increased excretion of nearly all amino acids, glucose, HCO3-, and PO4(3-). May result in metabolic acidosis (proximal renal tubular acidosis)
Bartter syndrome
AR, affects Na/K/2Cl transporter, results in hypokalemia and metabolic alkalosis with hypercalciuria
Gitelman syndrome
AR, reabsorptive defect of NaCl in DCT. Leads to hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria
Liddle syndrome
AD, Gain of function mutation causing increased Na reabsorption in collecting tubules (increased activity of epithelial Na channel). Results in hypertension, hypokalemia, metabolic alkalosis, decreased aldosterone. Tx: amiloride
Syndrome of apparent mineralocorticoid excess
Hereditary deficiency of 11-beta-hydroxysteroid dehydrogenase, which normally converts cortisol into cortisone in mineralocorticoid receptor containing cells before cortisol can act on the mineralocorticoid receptors. Causes hypertension, hypokalemia, metabolic alkalosis. Low serum aldosterone levels.
Actions of angiotensin II (6)
- acts at ATII receptors on vascular SM to cause vasoconstriction, 2. Constricts effect arteriole of glomerulus, 3. Increases aldosterone, 4. Stimulates ADH leading to H2O reabsorption, 5. Increases PCT Na/H activity, 6. Stimulates the hypothalamus (thirst)
How does the macula densa work?
Senses decreased NaCl deliver to DCT causes adenosine release, causes vasoconstriction
Where does Epo come from?
Interstitial cells in peritubular capillary bed
Where is vitamin D converted to its active form?
By the PCT cells
What do ADH and aldosterone regulate?
ADH regulates osmolarity, aldosterone regulares ECF volume and Na content
Effect of ANP
Causes increased GFR and increased Na filtration with NO compensatory Na reabsorption in distal nephron. Net effect: Na loss and volume loss
What causes K to shift out of cells?
Digitalis, hyperosmolarity, lysis of cells, acidosis, beta-blocker, high blood sugar (insulin deficiency) [DO LABS}
How do you monitor for too much magnesium?
DTRS (hypermagnesemia decreases DTRs), also causes lethargy, bradycardia, hypotension, cardiac arrest, and hypocalcemia
Respiratory compensation for metabolic acidosis
Winters formula. Pco2= 1.5[HCO3-] +8 +/-2
What can cause a metabolic alkalosis?
Loop/thiazide diuretics, vomiting, antacid use, hyperaldosteronism
What causes an anion gap metabolic acidosis?
MUDPILES: methanol, uremia, diabetic ketoacidosis, propylene glycol, iron tablets/isoniazid, lactic acidosis, ethylene glycol (oxalic acid), salicylates
What causes a normal anion gap metabolic acidosis?
HARD-ASS: hyperalimentation, addison disease, renal tubular acidosis, diarrhea, acetazolamide, spironolactone, saline infusion
Type 1 renal tubular acidosis
Distal, urine pH >5.5, defect in ability of alpha-intercalated cells to secrete H+ -> no new HCO3- is generated -> metabolic acidosis. Associated with hypokalemia, increased risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover)
Type 2 RTA
Proximal, urine pH
Causes of type 2 RTA
Fanconi syndrome and carbonic anhydrase inhibitors
Causes of type 1 RTA
Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract
Type IV RTA
Hyperkalemic, urine pH
What causes type IV RTA?
Decreased aldosterone production (e.g. diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency), or aldosterone resistance (e.g. K-sparing diuretics, nephropathy due to obstruction, TMP/SMX)
When do you see waxy casts?
End-stage renal disease/chronic renal failure
“Starry sky” granular appearance on light microscopy, “lumpy bumpy”
Acute poststreptococcal glomerulonephritis
Where are the immune complex deposits in APGN?
Subepithelial
Most impt prognostic factor for APGN?
Age
What do the crescents in RPGN consist of?
Fibrin and plasma proteins (ex. C3b) with glomerular parietal cells, monocytes, and macrophages
What diseases can lead to RPGN and what do you see with each of them?
Goodpasture- type II hypersensitivity, Ab to GBM, linear immunofluorescence; Granulomatosis with polyangiitis (Wegener)- PR3-ANC/c-ANCA; microscopic polyangiitis- MPO-ANCA, p-ANCA
What causes diffuse proliferative glomerulonephritis?
SLE or membranoproliferative glomerulonephritis
“Wire looping” of capillaries
DPGN
Where are the immune complex deposits in DPGN?
Subendothelial
What do you see in IgA nephropathy?
LM-mesangial proliferation; EM-mesangial IC deposits; IF- IgA based IC deposits in mesangium
What causes Alport syndrome?
Mutation in type IV collagen, causes thinning and splitting of glomerular basement membrane. Most commonly X-linked
“Basket weave” appearance on EM
Alport Syndrome
Sx of Alport syndrome
Eye problems, glomerulonephritis, sensorineural deafness
Where are the immune complex deposits in type I membranoproliferative glomerulonephritis?
Supendothelial
“Tram track” appearance on PAS and H&E stain
MPGN; Due to GBM splitting by mesangial ingrowth
Where are the immune complexes in type II MPGN?
Intramembranous
What are type I and type II MPGN associated with?
Type I may be 2/2 hepatitis B or C infection. Type II is associated with C3 nephritis factor (stabilizes C3 convertase causing decreased serum C3 levels)
Fatty casts
Nephrotic syndrome
Most common cause of nephrotic syndrome in AA and hispanics
FSGS
Most common cause of nephrotic syndrome in Caucasians
Membranous nephropathy
Where are the deposits in Membranous nephropathy?
Subepithelial
EM of membranous nephropathy
“Spike and dome” appearance with subepithelial deposits
Nephrotic presentation of SLE
Membranous nephropathy
LM of membranous nephropathy
granular
Diabetic glomerulonephropathy on LM
Mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)
How does diabetes cause kidney problems
Non-enzymatic glycosylation of GBM causes increased permeability and thickening; non-enzymatic glycosylation of efferent arterioles causes increased GFR causes mesangial expansion
Envelope shaped kidney stone
Calcium oxalate
Coffin lid shaped kidney stone
Ammonium magnesium phosphate (aka struvite)
Rhomboid or rosette shaped kidney stone
Uric acid
Hexagonal kidney stone
Cysteine
What is the test for cysteine stones?
Sodium cyanide nitroprusside test
Where does renal cell carcinoma arise from?
PCT cells
What paraneoplastic syndromes is RCC associated with?
Ectopic EPO, ACTH, PTHrP
Large eosinophilic cells with abundant mitochondria without perinuclear clearing
Renal oncocytoma, benign epithelial cell tumor
Cause of Wilms tumor
“Loss of function” mutation of tumor suppressor genes WT1 or WT2 on chromosome 11
What is Wilms tumor associated with?
Beckwith-Wiedmann: Wilms tumor, macroglossia, organomegaly, hemihypertrophy; WAGR: Wilms, aniridia, genitourinary malformation, mental retardation
CT findings in acute pyelonephritis
Striated parenchymal enhancement
Thyroidization of the kidney
Chronic pyelonephritis
Bone changes with renal osteodystrophy
Subperiosteal thinning of bones
What is ARPCD associated with?
Hepatic fibrosis
What is medullary cystic disease?
Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine. Medullary cysts usually not visualized; shrunken kidney on ultrasound. Poor prognosis
When is mannitol contraindicated?
Anuria, HF
Clinical uses for acetazolamide
Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri
Toxicity of acetazolamide
Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy
Toxicity of loop diuretics
Ototoxicity, hypokalemia, dehydration, allergy (sulfa), interstitial nephritis, gout
Which loop diuretic can be used in patients with a sulfa allergy?
Ethacrynic acid
Toxicity of thiazides
HYPER problems: hyperuricemia, hypercalcemia, hyperglycemia, hyperlipidemia; HYPO problems: hypokalemia, hypotension
What are the K sparing diuretics
Spironolactone and eplerenone; triamterene, and amiloride
MOA of spironolactone and eplerenone
Aldosterone receptor antagonists in cortical collecting tubule
MOA of triamterene and amiloride
Block Na channels in the cortical collecting tubule
Toxicity of ACE inhibitors
Cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations), increased Creatinine, Hyperkalemia, and Hypotension (especially watch for first dose hypotension)
Which drug is a direct renin inhibitor?
Aliskiren
When is Aliskiren contraindicated
In diabetics taking ACE inhibitors or ARBs
Which diuretics lead to acidemia and how?
Carbonic anhydrase inhibitors: decrease HCO3 reabsorption; K sparing: aldosterone blockade prevents K secretion and H secretion. Additionally, hyperkalemia leads to K entering all cells (via H/K exchanger) in exchange for H exiting cells
Which diuretics lead to alkalemia and how
Loop diuretic and thiazides. Volume contraction increases AT II, increases Na/H exchange in PCT, increased HCO3 reabsorption. K loss leads to K exiting all cells (in exchange for H entering cells). In low K state, H (rather than K) is exchanged for Na in cortical collecting tubule causing alkalosis and “paradoxical aciduria”
