Renal Flashcards
Kidney artery tree
Renal, segmental, interlobar, arcuate, interlobular
12th rib fracture lacerates what structure?
Kidney
Ureteric bud derivatives
Collecting system, including collecting tubules and ducts, major/minor calyces, renal pelvic, and ureters
Metanephric mesoderm/blastema derivatives
Glomeruli, Bowman’s space, proximal tubules, loop of Henle, and distal convulted tubulues
Post-streptococcal GN: histo
Subepithelial humps (electron-dense deposits on epithelial side of GM), composed of IC made up of IgG, IgM, C3
Crescentic GN: histo
Prominent fibrin deposition
Renal cancer RF
Tobacco smoke, obesity, HTN
Bladder cancer RF
Tobacco smoke, occupational exposure to rubber, textiles, leather
Renal angiomyolipoma
Benigh tumor comporised of blood vessels, smooth muscles, and fat; bilateral renal angiomyolipomas are associated with tuberous sclerosis (AD)
Uric acid crystallization occurs in what structure, and is prevented by what?
Collecting duct (2/2 low urine PH); thus, give hydration and urine alkalinization to prevent
GFR is estimated by calculating the clearance of what substance?
Inulin
PAH
Freely filtered at glomerulus, and secreted into the urine at the proximal tubule (thus, excretion > filtered load)
Calcineurin
Protein phosphatase that, once activated, dephosphorylates NFAT and allows the latter to bind the IL-2. IL-2 stimulates growth and differentiation of T-cells. Inhibit with cyclosporine or tacrolimus.
Oxybutynin
Antimuscarinic agent used for urge incontinence
Post-op urinary retention rx
Bethanechol (muscarinic agonist)
GRE and creatinine relationship
If GFR normal, relatively large decreases will only result in small increases in Cr. If GFR is significantly decreased, small decreases will produce relatively large increases in Cr. Every time GFR is halved, Cr doubles.
Left and right renal vein differences
Left renal vein drains the left suprarenal vein (obstruction causes varicocele) and the left gonadal vein
Amphotericin B MOA, SE
Binds to ergosterol in fungal cell membranes to form holes; Nephrotoxicity causing severe hypokalemia and hypomagnesemia
Sudden onset of abdominal/flank pain, hematuria, L-sided varicocele
Renal vein thrombosis
Furosemide MOA
inhibit Na-K-2Cl symporter @ loop of Henle, causing increased Na, Cl, fluid excretion; and stimulate prostaglandin release (NSAIDs will thus blunt diuretic effect)
UTI pathogenesis
Suppression of endogenous flora, colonization of distal uretrha by pathogenic gram-negative rods, and attachment of such pathogens to bladder mucosa
What is necessary for development of acute pyelonephritis?
Anatomic or functional vesicoureteral reflux
PT: what substrates increase in concentration?
PAH, creatinine, inulin, urea
PT: what substrates do not change in concentration?
Na, K
PT: what substrates decrease in concentration?
Bicarb, glucose, AA
Furosemide SE
Hypokalemia, hypomagnesemia, hypocalcemia; ototoxicity
Clear cell carcinoma
Renal tubular cells; histo: rounded/polygonal cells with abundant clear cytolasm with high glycogen or lipid content
Visual impairment of HIV pt; rx, SE?
CMV-induced retinitis; ganciclovir, foscarnet; foscarnet SE: hypocalcemia (chelates with Ca), hypomagnesemia (nephrogenic wasting)
Calcium stone prevention
Ample fluid intact, high-normal calcium intake, low-protein diet, low-sodium diet
Calcium stones with hyperoxaluria
Vitamin B6 (decreases endogenous oxalate production)
ACE SE
first-dose hypotension (esp with pts with hyponatremia, hypovolemia 2/2 existing diuretics, low baseline BP, high renin/aldosterone lvels, renal impairment and heart failure)
The majority of water reabsorption occurs where?
Proximal convoluted tubule
Goodpastures: LM, IF
Glomerular crescent formation; linear deposits of IgG and C3 along glomerular BM
Membranous glomerulopathy: LM, IF
Diffuse capillary wall thickening; granular deposits of IgG/C3 along glomular BM
Alport syndrome pw, EM
Nephritis, deafness; BM splitting
MPGN: EM, IF, LM
EM: BM splitting, granular deposits, lobular appearance with proliferating mesnagial cells and increased mesangial matrix
Mannitol MOA, SE
Osmotic diuresis, agent to lower intracranial pressure; pulmonary edema 2/2 reactionary volume expansion
Renal osteodystrophy MOA
ESRD-related retention of phosphate and decreased synthesis of calcitriol causes hypocalcemia, secondary hyperparathyroidism and renal osteodystrophy
Renal cell carcinoma gene mutation
VHL deletion on C3p (mostly sporadic)
MOA of hypocalcemia in renal failure
Decreased calcitriol leads to decreased Ca, phosphate absorption from intestine and kidneys; decreased urinary excretion of phosphate leads to elevated serum phosphate, and this phosphate binds with Ca and reduces serum Ca; Thus, low serum calcium and high phosphate
Calcium oxalate crystals in urine: appearance, significance
Folded envelopes on microscopy; ethylene glycol ingestion (AG acidosis, osmolar gap)
Urachus
Remnant of allantois that connects bladder with yolk sac during fetal development; failure of urachus to obliterate leads to urine discharge from the umbilicus
ATN most likely to occur in what areas of the nephron
Tubular epithelial cells in proximal tubules and the thick ascending limb of Henle’s loop; muddy brown casts are pathognomonic for ATN
Finasteride and terazosin different timeline of action
Finasteride: 6-12 months; terazosin: days-weeks
Angiotensin II: two negative feedback systems on RAS
Stimulates juxtaglomerular cells to inhibit renin release; and elevates BP/Na to decrease renin reliease via intrarenal baroreceptors and macula densa
K flow throughout nephron
Most resorbed by the proximal tubule and loop of Henle; K depletion stimulates alpha-IC cells to reabsorb extra K via H/K ATPase; high K leads principal cells to secrete K
Proximal 1/3 of ureter receives its blood supply from what artery?
Renal artery
Drug-induced interstitial nephritis: presentation
Fever, maculopapular rash, and oliguria 1-3 weeks after starting treatment with beta lactam, NSAD, sulfonamides, rifampin, diuretics; peripheral eosinophilia and eisinophiluria are important clues
AD polycystic kidney disease
pw HTN, flank pain, gross hematuria, UTI, kidney stones; Numerous kidney and liver cysts seen by the 3rd or 4th decade help make diagnosis; most common hereditary cause of renal failure (age 70)
Nephrotic syndrome pw, difference between highly/poorly selective proteinuria
Massive proteinuria (>3.5 gm/day), hypoalbuminemia, generalized edema, hyperlipidemia, lipiduria; highly selective (minimal change dz with low molecular weight proteins, such as albumin and transferrin)
Most common cause of fetal hydronephrosis
Inadequate recanalization of the ureteropelvic junction
Most common cause of calcium kidney stone disease
Idiopathic hypercalciuria with normal serum calcium levels
Hyperoxaluria
Diet high in oxalate (chocolate, nuts, spinach), low calcium diets, CD/intestinal malabsorption
Hyperuricosuria
High protein diet
Hyperuricemia and hyperuricosuria
Myeloproliferative disorder or tumor lysis syndrome; typically stimulates calcium oxalate formation (uric acid stone less common)
Metabolic acidosis: kidney correction MOA
- Increased bicarb reabsorption at the proximal tubule (via carbonic anhydrase action in the lumen); 2. Increased H secretion throughout nephron (Na/H antiporter in proximal nephron, H-ATPase, H/K ATPase in alpha-IC cells; 3. Increased acid buffer execretion (NH3 (more important, at proximal tubule) and HPO4)
GFR, RPF, FF
Renal plasma flow is the amount of plasma delivered to the kidney per unit of time, esimated by PAH; GFR depends on hydrostatic/oncotic pressures and is calculated separately
Cystinuria
AR Inborn defect of the transporter for cystine, ornithine, aginine, lysine; pw nephrolithiasis that presents with renal colic in 2/3rd decades, with UA showing hexagonal cystine crystals
Horseshoe kidney
Isthmus lies posterior to the IMA
Renal cell carcinoma
Arise from epithelial cells of the proximal renal tubules; grossly, golden yellow mass and light microscopic exam, cells with abundant clear cytoplasm and eccentric nuclei
ARB MOA
Block AT-1 receptor and inhibit ATII, resulting in arterial vasodilation and decreased aldosterone secretion
PSGN
- enlarged, hypercellular glomeruli on light microscopy; 2. “lumpy-bumpy” granular deposits of IgG and C on IF; 3. electron-dense deposits on the epithelial side of basal membrane
Spironolactone similar to what molecule
Steroids, so can cause gynecomastia, decreased libido, impotence
Bladder outflow obstruction leads to what?
Reflux nephropathy, hydronephrosis, renal interstial atrophy and scarring
ADH effect on urea reabsorption
Increases passive urea transporters in the inner medullary collecting duct, allowing highly concentrated urea to diffuse down its gradient into the medullary interstitum and further into the thin loop of Henle (contributing to osmotic gradient)
Clearance
(Urine concentration/plasma concentration) X urine flow rate)
RBF two ways of calculating
(Renal artery pressure - renal vein pressure)/renal vascular resistance; (PAH clearance)/(1-hct)
Membranous glomerulopathy
Mostly idiopathic; but can be a.w. malignant tumors, infections (Hep B, C), meds; light microscopy shows diffuse increased thickness of the BM (without increased cellularity), “spike and dome” appearance on silver stain; IF shows granular deposits
Total filtration rate of substance A
Inulin clearance x plasma concentration of substance A
IgA nephropathy
pw painless hematuria 2-3 days after URI; IF: Prominent IgA deposits in the mesangium; EM: electron dense material in mesangium
Henoch-Schonlein disease
Purpuric lesions on extensor surfaces; GI (ab pain, intestinal bleeding, intussusception; IgA nephropathy
Salicylate poisoning
Acute respiratory alkalosis followed by metabolic acidosis
NSAID associated chronic renal injury
Papillary necrosis and chronic interstitial nephritis with mild/no glomerular and vascular abnormalities
Cystinuria pw, rx
Recurrent stone formation at young age; hexagonal cystine crystals on UA; sodium cyanide-nitroprusside test detects cystine’s sulfhydryl groups
Acute rejection of transplants: rx
Anti-CD3 antibodies (muromonab) that inhibit t-lymphocytes
MM nephropathy
Bence jones proteins precipitate with Tamm Horsfall protein and form eosinophilic casts (not eosinophil cell casts) that compress tubular epithelium and obstruct tubular lumens and impede renal function; LM: numerous large, glassy eosinophilic casts in tubular lumen
Determinants of diffusion across semipermeable membrane directly proportional with, and inversely proportional with
concentration difference across membrane, total surface area, solubility of substance; membrane thickness and molecular weight of the molecule
ATN clinical course
Initiation; maintenance (oliguria for 1-2 weeks, granular casts, flattening/necrosis of tubular epithelial cells): recovery: re-epithelization of tubules (polyuria, normalizatin of GFR)
Long-standing nonmalignant HTN or DM pw
Homogenous deposition of eosinophilic hyalin material in the intima and media of small arteries and arterioles characterizes hyaline arteriolosclerosis
Malignant HTN
hyperplastic arteriolosclerosis (homogenous, onion-like concentric thickening of the arteriole wall)
Important prognostic factor in PSGN
Age (95 percent of children, 60 percent of adults recover completely)
Idiopathic membranous nephropathy a.w.
Circulating IgG4 antibodies to phospholipase A2, leading to IC deposition in glomerulonephritis
Minimal change disease
Immune dysregulation and overproduction of a specific cytokine that directly damages podocytes, leading to effacement and fusion of food processes; selective loss of albumin in the urine (but not other serum proteins)
Glaucoma pw
Severe unilateral eye pain and ipsilateral HA with severe nausea and “halo” around objects
Kidney stones: calcium oxalate or calcium phosphate
70-80%, radiopaque, colorless octahedron
Struvite (magnesium ammonium sulfate or triple phosphate)
15%, radiopaque, rectangular prism (“coffin lids”); associated with urease-forming UTI organisms (proteus), “staghorn” calculi,
Uric acid
Radiolucent; yellow/red-brown, diamond or rombus
Cystine
Flat, yellow, hexagonal;
Pelvic surgery risks
Ureter ligation and hydronephrosis
Anatomy: ureter course
Cross over the common/external iliac vessels and under the gonadal vessels (and uterine vessels in females); anterolateral to the internal iliac vessels and medial to the ovarian vessels
Digoxin toxocity in elderly patients
Reduce dose 2/2 age-related renal insufficiency (even with normal creatinine)
ANCA-associated RPGN
Pw with renal failure, pulmonary symptoms, upper respiratory symptoms (Granulomatous polyangitis); crescents on light microscopy; absence of Ig or C3 deposits
ATN: initiate stage
Ischemic injury to tubules precipitated by hemorrhage, acute MI, sepsis, surgery
ATN: maintenacne
Decreased output, fluid overload, increasing creatinine/BUN, hyperkalemia
ATN: Recovery
Gradual increase in urine output leading to high-volume diuresis. Electrolyte abnormalities, including decreased K, Mg, PO4, Ca 2/2 decreased tubular function
WBC cast formation
WBC precipitated by Tamm-Horsfall protein secreted by tubular epithelial cells; when accompanied by systemic symptoms, means acute pyelonephritis; if no urinary symptoms, could be acute interstitial nephritis
Muscarinic receptors: M1
Gq, Brain, memory formatoin/cognitive functioning, confusion
Muscarinic receptors: M2
Gi, heart, decreased HR and decreased ionotrophy; increased HR and contractility
Muscarinic receptors: M3
G1: Lung (bronchoconstriction), bladder (detrusor contraction), eyes (miosis, accomodation), GI (increased peristalsis, increased salivary and gastric secretions), skin (increased sweat production)
Diabetic nephropathy MOA
Glomerula hyperfiltration and increased in mesangial matrix/thickening of GBM; affects the glomeruli and the arterioles; nodular glomerulosclerosis (i.e. KW nodules), diffuse glomerulosclerosis, and hyaline arteriolosclerosis
Nephritic vs nephrotic
Former: HTN, mild proteinuria (3.5 g/day), lipiduria, absence of RBC casts in the urine, normal renal function
Crescent formation
Glomerula parieta cells, monocytes, macrophages, fibrin; eventually become sclerotic, disrupting glomerular function and causing irreversible renal injury
Hemolytic uremic syndrome MOA
Shiga toxins from E Coli O157:H7 or Shigella injure the endothelium of preglomerular arterioles and glomerular capillaries, leading to platelet activation (thrombocytopenia) and formation of microthrombi (microangiopathic hemolytic anemia). Dmg to renal vasculature results in AKI
Papillary necrosis etiologies
SCD or trait, DM, analgesic nephropathy, severe obstructive pyelonephritis; acute colicky flank pain, gross hematuria, passage of tissue fragments in urine
