Renal Flashcards
Highly selective proteinuria
Mostly low MW protein excretions; Minimal-change disease - defect in negatively charged molecules in GBM –> inability to repel albumin (also transferrin)
ACEi work how?
Decrease angioI->angioII, which blocks arteriolar vasoconstriction and aldosterone secretion. Ultimately lead to increased renin. B/c ACE breaks down bradykinin, increased bradykinin level.
Substances with no tubular absorption or secretion
Inulin and mannitol
Substances with net tubular secretion?
PAH (almost all secreted at PROXIMAL tube) and creatinine
Crescent formation pathogenesis?
Diagnostic for rapidly (wks-months) progresive glomerulonephritis. Dmg to BM lead to gaps where macrophages, T-cells, FIBRIN go into Bowman’s space. Fibrin deposition leads to parietal cell proliferation = crescent. Linear deposits of immunoglobulin.
Renal papillary necrosis associated with?
Sickle cell disease/trait. Analgesic nephropathy (e.g. phenacetin), DM, Acute pyelo or UT obstruction. Gray-white/yellow necrosis at distal renal pyramids. Coag infarct. Abrupt gross hematuria, colicky flank pain b/c of ureteral obstruction 2/2 sloughed papillae.
RPGN types?
Type 1 = anti-GBM. associated with Goodpasture syndrome. Immuno w/ IgG and C3 deposits (Type II HS). Type 2=IC-mediated 2/2 post-strep, SLE, IgA or Henoch-Schonlein….Type 3 = “pauci immune” w/ ANCA. Associated with Wegener’s.
Goodpasture’s
Anti-GBM (alpha-3 chain of collagen type IV). RPGN (crescents) and pulmonary hemorrhages.
Aldosterone
Synthesized and released by zone glomerulosa cells. Stimulated by angiotensin II and high serum K+. Promotes K+ secretion from principal cells and H+ secretion of intercalated cells of renal collecting tubules.
Drug that acts on proximal tubule
Acetazolamide - Carbonic anhydrase inhibitor. Drug blocks NaHCO3 reabsorption -> self-limited diuresis. Used for acute angle-closure glaucoma for dec. aqueous humor formation, metabolic alkalosis, pseudo tumor cerebra. Tox -hyperchloremic metabolic acidosis, parasethesias, NH3 fox, sulfa allergy
Drug that acts on descending Henle
Mannitol, an osmotic diuretic. Very permeable to water.
Drug that acts on thick ascending limb of Henle?
Loop diuretics (e.g. furosemide) Inhibits Na-K-2Cl symporters leading to increased Na, Cl-, and H2O excretion + Ca excretion.
Drug that acts on distal convoluted tubule
HCTZ. Impermeable to water and transports Na+ and Cl-.
Drugs that work on collecting duct?
K+ sparing diurects. Aldo receptor antagonists and amiloride (Na+ channel blocker)
RCC path
From renal tubular cells. Rounded or polygonal cells w/ abundant clear cytoplasm b/c had glycogen and lipids
Thiazide side effects
Decrease intravascular volume leads to aldo leads to excretion of K+ and H+ -> HypoK and metabolic ALKalosis. Hyponatremia. Hyperuricemia b/c of uric acid reabsorption in proximal tubules. HLD. Impaired carb tolerance. Hypercalcemia, hyperglycemia.
Role of mesonephros vs. metanephros?
Meta is SO VERY real. Mesonephros = interim kidney for 1st TM + ureteric bud –> ureter, pelvis, calyces, COLLECTING ducts by wk 10. Metanephros starts in wk 5. Metanephric mesenchyme interacts with ureteric bud to induce formation of glomerulus to distal convoluted tube. Last part of canalization is uretopelvic junction.
Pronephros?
Degenerates by wk 4.
Etios of Potter sequence
ARPKD, posterior urethral valves, b/l renal agenesis
Horseshoe kidney
Fusion of inferior poles. Then get trapped as ascend from pelvis by INFErior mesenteric artery. Increased risk of ureteropelvic junction obstruction, hydronephrosis, renal stones, Wilms. Associated with TURNER’s syndrome.
Multicystic dysplastic kidney
Etio is poor metanephric mesenchymal interaction with ureteric bud -> nonfunctional kidney of cysts and connective tissue. Often asymptomatic and unilateral due to hypertrophy of other kidney.
Interlobular artery vs. interlobar artery vs. arcuate artery?
Interlobar artery on either side of medullary pyramid. Arcuate arteries on cortical side. interlobular artery extend towards cortex.
Superficial cortical nephrons vs. juxtamedullary nephrons
Superficial cortical have glomeruli in outer corex with SHORT loops only descend to outer medulla. Juxtamedullary nephrons have glomeruli near corticomedullary border, larder glomeruli, LONG loops of Henle deep into papilla. Also have vasa recta, peritubular capillaries which follow loops
Where are juxtaglomerular cells compared to mesangial cells?
Juxtaglomerular cells located between afferent arteriole and macula dense (inward facing cells of distal renal tubule). Mesangial cells in the glomerulus.
Water under the bridge
Ureters under UTERINE artery and DUCTUS deferens.
What do I need to know about fluid compartments?
60-40-20 rule: 60% of body weight is water. (40% or 2/3 is ICF and 20% or 1/3 is ECF). 60-40-15-5 rule (5% or 1/4 of ECF is plasma volume and 15% or 3/4 of ECF is interstitial fluid).
How do you measure plasma volume and ECF volume?.
Radiolabeled albumin and inulin respectively.
Renal clearance
= volume of plasma cleared of a substance per unit time = substance clearance / plasma concentration = Urine conc. of X * urine flow rate / plasma concentration of X
What is glomerular filtration composed of?
Fenestrated capillary epithelium = size. Fused BM w/ HEPARAN sulfate = NEGATIVE charge barrier (lost in nephrotic syndrome -> albuminemia, hypoproteinemia, edema, hyperlipidemia). Epithelial layer of podocyte foot processes
GFR
Normally ~ 100 mL/min. Creatinine clearance slightly overestimates GFR b/c of slight secretion by renal TUBULES. GFR = [inulin]u x V / [inulin]p = Kf [ net hydrostatic pressure - net oncotic pressure)]
Renal PLASMA flow vs. renal BLOOD flow?
RBF > RPF b/c renal blood flow includes all the extra VOLUME of RBC’s
Renal plasma flow
Estimated w/ renal clearance of para-aminohippuric acid (PAH), which is filtered and secreted, and nearly ALL is EXCRETED. Therefore, eRPF = [PAH]u * V / [PAH]plasma. Estimates true RPF from Fick principle (with plasma conc. = renal artery - renal vein concentration, since no other organ extracts PAH and remain vein concentration = 0). eRPF underestimated by ~10% b/c renal vein conc. is NOT 0.
Renal blood flow
= RPF / (1 - Hct).
Filtered load?
mg/min = GFR (mL/min) x plasma concentration (mg/mL)
Filtration fraction (FF) =
GFR / RPF
Effects of arteriolar constriction on RPF, GFR, and FF?
Afferent constriction - dec. RPF, dec. GFR, - FF. Efferent constriction - dec. RPF, inc. GFR, inc. FF.
Glucose clearance?
At normal plasma lvls, glucose is completely reabsorbed at PROXIMAL tubule w/ Na+/glucose CO-transporter. At ~200 mg/dL glycosuria begins. At ~375 mg/dL, co-transporters are fully saturated. In pregnancy, reabsorption of aa’s and glucose in prox tubule down -> glycosuria and aminoaciduria
Amino acid clearance?
By proximal tubule with sodium-dependent transporters. Hartnup disease - Pellagra-like symptoms because these transporters can’t reabsorb leading to neutral aminaciduria and decreased aa absorption in gut. Tx = high-protein + nicotinic acid
Early PCT
Reabsorbs glucose, aa’s, phosphate/lactate/citrate with Na-X co-transporters. Reabsorbs 65-80% Na+ and 85% HCO3 with Na-H exchange and Carbonic anhydrase system. AT-II stimulates exchange –> reabsorbed Na+, HCO3, and water -> contraction alkalosis. PTH inhibits Na-Phos co-transport –> exertion of phosphate –> inc. Ca+ serum. Slightly NEGative lumen. Iso-osmotic water absorption.
Late PCT
High Cl-, no glucose, no aa, no HCO- enters. Na-H and Cl-FORMATE- exchanger AND paracellular absorption of NaCl via tight junctions –> Reabsorption of NaCl and water absorption. Iso-osmotic water absorption.
What drives reabsorption?
High oncotic pressure of peritubular capillary blood. The higher the GFR the higher the oncotic pressure, meaning that increased GFR leads to increased reabsorption (glomerulotubular balance). Balance upset by ECF volume changes (inc ECF -> decreased fractional reabsorption).
Thin descending and ascending loop of Henle
Descending loop is HIGHLY permeable to water and solutes while Ascending loop is NOT permeable to water. Medulla is hypertonic. So water moves out of thin descending, and solutes move INTO thin ascending —> concentrating/hypertonic urine
Thick ascending loop of Henle
ACTIVE reabsorption of Na+ (25%) in a LOAD-dependent fashion but NO water reabsorption. (This is why diuretics affecting proximal tube are mild b/c this part of loop makes up for it). Na-K-2Cl co-transporter driven by Na+ gradient. Reabsorption via Na-K ATPase (Na) and diffusion (K, Cl). Some K+ goes back to lumen = lumen-positive! Loop diuretics bind to Cl- portion. This is the DILUTING segment. Indirect paracellular reabsorption of Mg and Ca b/c of positive lumen.
Early distal convoluted tubule
Reabsorbs 5% of Na+ and Cl- via Na-Cl co-transporter (via Na+ gradient) in LOAD-dept fashion. Thiazide diuretics bind to Cl- site. IMPERMEABLE to water = “cortical dilutnig segment.” PTH increases Ca-Na exchange -> Inc Ca reabsorption. Used for HTN, CHF, idio hypercalciuria, nephrogenic DI, osteoporosis
Late distal convoluted tubule/Collecting Duct
Principal cells and alpha-intercalated cells. Principal - 3% Na+ reabsorption via channels (ENaC) under HORMONAL control. Aldosterone induces transcription of ENaC,Na-K ATPase, and enzymes of TCA cycle. Inhibited by K+-sparing diuretics (e.g. amiloride & triamterene block ENaC, spironolactone - which blocks aldo entering nucleus). Principals also secrete K+ and H+. ADH acts at V2 receptor to INSERT AQUAPORIN. Alpha-intercalated reabsorb K+ and excrete H+.
Fanconi syndrome
Frank is 1st. Reabsorption defect of PCT. Excretion of AAs, glucose, HCO3-, phosphate –> metabolic acidosis. etios - Wilson, ischemia, nephrotoxins/drugs
Renal Tubular Defects?
Fanconi, Barterr, Gitelman, Liddle. “F(r)ank and Bart Git Little Renal Tubules.”
Barterr syndrome
Bart is 2nd. Reabsorption defect of thick ascending Henle. AR affecting cotransporter -> hypokalemia, metabolic alkalosis, and hypercalciuria (stops paracellular)
Gitelman syndrome
Git is 3rd. Rebasorption defect of NaCl in DCT. AR and less severe than Barterr -> hypokalemia, metabolic alkalosis W/O hypercalciuria
Gitelman syndrome
Git is 3rd. Rebasorption defect of NaCl in DCT. AR and less severe than Barterr -> hypokalemia, metabolic alkalosis, hypocalciuria
TF/P?
Concentration of substrate in tubular fluid / conc. in plasma. TF/P = 1.0 is NO net reabsorption or secretion (e.g. Bowman’s space for freely filtered substance). TF/P < 1.0 is NET reabsorption relative to water. TF/P > 1.0 is NET secretion relative to water. (or less reabsorption compared to water).
The Many effects of AT-II
Hypothalamus - increases thirst and stimulate secretion of ADH -> inc. aquoporin insertion in principals cells. Vasculature - vasoconstriction via AT-II receptor. Adrenals - stimulates aldo release –> ENaC synthesis at principals cells of DCT/CT. Kidney - stimulates Na-H exchange at PCT -> Na+, HCO3, and water reabsorption. Constriction of efferent arteriole of glomerulus –> (inc GFR but dec RPF) increased FF. Limits baroreceptor thereby limiting reflex brady
Angiotensinogen, Renin, ACE are made?
Liver, Juxtoglomerular apparatus, Lung/kidney
What stimulates renin production?
Decreased Bp sensed by JG cells, decreased Na+ delivery (macula dense cells), or INC sympathetic tone (B1-receptors). All parts called the “Juxtoglomerular apparatus.”
ANP?
Released from atria b/c of INC volume. Relaxes vascular SMC via cGMP. Increased GFR, increased Na+ filtration w/o reabsorption –> NA+ LOSS and volume loss
EPO made where?
Interstitial cells in PERITUBULAR capillary bed in response to HYPOXIA
1,25-(OH)2 Vitamin D production?
Proximal tubule cells convert 25-OH D to 1,25 D with 1alpha-hydroxylase stimulated by PTH
Prostaglandins in the kidney?
Paracrine secretion vasodilates the afferent arterioles to increased RBF. NSAIDs block this renal-protective mechanism -> decreased GFR and ARF. Loop diuretics stimulate release of renal prostaglandin -> inc. RBF -> inc. GFR.
Mechanistic etios of hyperkalemia?
DO Insulin LAB work = Digitalis, hyperOxmolarity, Insulin deficiency, Lysis of cells, Acidosis, Beta blockade
Mechanistic etios of hypokalemia
Hypo-osmoarlity, Insulin (via inc. Na-K ATPase), Alkalosis, Beta-agonist,.
Symptoms of hyperNa vs. hyorNa?
Hypo - nausea, malaise, stupor, coma. Hyper - irritability, stupor, coma. In other words, roughly the same.
Symptoms of hyperK vs. hypoK?
Hyper - Wide QRS, PEAKED T-waves, arrhythmias, muscle weakness. Hypo - U waves, flattened T waves, arrthythmias, muscle weakness.
Symptom of hyperCa vs. hypoCa
HyperCa - Stones, bones, groans (ab pain), PSYCH. HypoCa - tetany, sz, QT prolongation
Symptoms of hyperMg vs. hypoMg?
HyperMg - decreased reflexes, brady, hypotension, cardiac arrest, hypoCa. HypoMg - tetany, torsades
Symptoms of hyperPhos vs. hypoPhos?
HyperPhos - renal stones, metastatic calcifications, hypoCa. HypoPhos - bone loss, osteomalacia
Metabolic acidosis equation for respiratory compensation?
Winters; PCO2 = 1.5 [HCO3] + 8 +/- 2.
Metabolic acidosis types
AG = Na - (Cl- + HCO3). High AG = MUDPILES while Normal AG = HARD-ASS.
MUDPILES
Methanol, Uremia, DKA, Propylene glycol, Iron tablets/INH, Lactic acidosis, Ethylene glycol, Salicylates (late)
HARD-ASS
Hyperalimentation, Addison disease, RTA, Diarrhea, Acetazolamide, Spironolactone, Saline infusion
Type 1 RTA
Defect of H+ secretion of alpha-intercalated cells. Associated with hyperkalemia and metabolic acidosis. Increased risk for CaPho kidney stones. Etios - amphotericin B tox, analgesic nephropathy, multiple myeloma (light chains), congenital abnls or urinary tract. 1A (acid and alpha), 2B (bicarbonate at proximal), 4D(alDO).
Type 2 RTA
Defect in proximal HCO3 reabsorption -> metabolic acidosis. Urine is acidified in DCT -> ph < 5.5. Hypokalemia. Increased risk for hypophosphatemic rickets. Causes - Fanconi syndrome, Lead, amino glycosides, CA inhibitors. “1A 2B 4D”
Type 4 RTA
Hypoaldosteronism, aldo resistance, or K+ sparing diuretics —> HYPERKalemia -> impairs ammoniagenesis in proximal tubule -> decreased buffering capacity and decreased H+ excretion into urine. “1A 2B 4D”
Conn syndrome
Primary hyperaldosteronism 2/2 aldosterone secreting tumor -> HTN, hypokalemia, metabolic alkalosis, and decreased plasma renin activity. Tx with aldosterone antagonist like spironolactone or eplerenone. “I AM KAHN is a little hyperaldo’ed.”
Post-strep glomerulonephritis clinical
Child w/ fever, nausea, cola-colored 2-3 wks after strep skin/throat. Dysmorphic red cells, RBC casts, mild proteinuria. Type III (IC). Increased anti-DNase B and DEC. complement levels. Tx = loop diuretics and vasodilators for edema and HTN. AGE is best prognostic factor. Only 60% of adults will resolve completely.. GAS. IC-mediated.
How does ESRD affect Ca+ balance?
Both decreased formation of Vit D and phosphate RETENTION leading to HYPERphosphatemia —> hypocalcemia. Hyperphosphatemia and hypocalcemia –> inc. PTH synthesis and hyperplasia = secondary hyperparathyroidism
Why do we care about casts in UA?
B/c it tells us that pathology is in the kidney NOT the bladder.
RBC vs. WBC casts
Glomerulonephritis, ischemia, or malignant HTN vs. tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
ATN casts?
Granular “muddy brown”
Nephrotic syndrome casts?
Fatty casts. “Oval fat bodies.”
CRF casts?
Waxy casts
Hyaline casts?
Non-specific, can be normal often in concentrated urine samples.
Primary glomerular vs. secondary glomerular disease?
Primary only involves glomeruli (e.g. Minimal change). Secondary involves glomeruli and other organs (e.g. SLE, diabetic nephropathy)
Nephritic syndrome glomerular etios?
Acute post-strep glomerulonephritis, RPGN, Berger (IgA glomerulonephropathy), Alport syndrome. Both - diffuse proliferative glomerulonephritis and membranoproliferative glomerulonephritis
Nephrotic syndrome glomerular etios?
FSGS, Membranous nephropathy, Minimal change, amyloidosis, diabetic glomerulonephropathy. Both - diffuse proliferative glomerulonephritis and membranoproliferative glomerulonephritis
Focal segmental glomerulosclerosis path?
Light - segmental sclerosis and hyalinosis. Immuno NEG. EM - effacement of foot processes like in minimal change disease
FSGS clinical
Most common cause of nephrotic syndrome (AA’s and Hispanics). Etios - etio, associated with HIV, SCD, heroin, massive obesity, IFN, CKD). Prog - inconsistent, may progress
Membranous neuropathy path?
Light - Uniform, diffuse THICK of glomerular capillary wall w/o increased cellularity. IF - granular deposits b/c of IC’s. EM - Spike and dome on methenamine silver stain.
Membranous neuropathy clinical
Most common cause of 1’ nephrotic in Caucasian adults. Etio - 85% idio (Ab to PLA2), o/w SLE, infections, SLE. Prog - poor response to steroid -> may progress
Minimal change disease path?
Light - NORMAL. IF NEG. EM = Effacement of FOOT processes.
Minimal change disease clinical
Most common in children. Triggered by infection, immunization, or immune stimulus. Associated with Hodgkin’s. Prog = Excellent with corticosteroids Edema, Na+ and water retention, increased cholesterol, TGC’s, lipoproteins, etc. 2/2 to liver compensation for drop in oncotic pressure.
Amyloidosis renal path?
LM - Congo red w/ APPLE-green briefing. Associated with MM, TB, RA.
Membranoproliferative glomerulonephritis path?
Type I - subendothelial IC deposits w/ ‘tram-track” appearance b/c of GBM splitting + Mesangial proliferation. Granular IF. Type II shows intramembranous IC deposits.
Membranoproliferative glomerulonephritis clinical
A nephritic syndrome that can also look nephrotic. Type I associated with HBV, HCV, or idil. Type II associated with c3 nephritic factor.
Diabetic glomerulonephropathy path
Light - MESANGIAL expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesions). Glycosylation of GBM -> thickening and increased permeability. Glycosylation of efferent arterioles -> increased GFR and mesangial expansion.
Acute post streptococcal glomerulonephritis path?
Light - hyper cellular and enlarged glomeruli. IF - “Starry sky” or “lumpy bumpy” b/c of IgG, IgM, and C3. EM - eubepithelial IC humps.
Diffuse proliferative glomerulonephritis (DPGN)
Due to SLE or MPGN. Light - wire-looping of capillaries. EM - Subendothelial and sometimes intramembranous IC’s. IF - granular.
IgA nephropathy
Light - mesangial proliferation. EM - mesangial IC deposits. IF - IgA-based IC deposits in mesangium. Presents w/ URI or acute gastro. Episodic hematuria with RBC casts.
Alport syndrome
THINNING and plotting of GBM b/c of mutation in type IV collagen. DEAFNESS and EYE problems.
Only radiolucent stone?
Uric acid
Calcium stones
Phosphate or oxalate. Radiooaque, envelop or dumbell shaped. Phosphate precipitate at high pH while oxalate precipitates at low pH. Promoted by hypercalciuria. Oxalate crystal 2/2 to ethylene glycol, vitamin C, Crohn’s. Tx for recurrent = thiazides and citrate.
Ammonium magnesium phosphate stones
Struvite stones. Precipitate at high pH. Radiopaque Coffin lid. Etio - infection with Urease + bugs (Proteus, Staph, Klebs) -> hydroxylsis of urea to ammonia -> alkalization. Tx infection and surgical removal.
Stones that precipitate at high pH vs. low pH?
High pH are calcium phosphate, ammonium magnesium phosphate. Low pH are calcium oxalate, uric acid, and cystine. High on phosphate and struvite. OX is low to the ground.
Uric acid stones
Radiolucent rhomboid or rosettes. Precipitate at low pH (e.g. collecting tubules). RF are low urine volume, arid climates, acidic pH. Visible on CT and US but not X-ray. Association with gout or high cell turnover (leukemia). Tx = alkalization of urine
Cystine stones
Hexagonal. Radioopaque and low pH precipitating. Children 2/2 to cystinuria. Staghorn calculi. Na nitroprusside test is positive. Tx = alkalinize urine
Hydronephrosis
Distention of renal pelvis and calyces 2/2 urinary tract obstruction (stones, BPH, cervical ca, ureter injury) or retroperitoneal fibrosis and vesicouretral reflux. Compression atrophy of renal cortex an dmedulla.
Renal cell carcinoma
Arising from PROXIMAL TUBULE –> polygonal clear cells w/ accumulated lipids and carbs. Men 50-70’s w/ smoking and obesity. Usually symptoms late in course (hematuria, flank pain, palpable abdominal mass), fever, malaise, anorexia, wt loss. Mets to lung and bone via renal vein to IVC. Paras include polycythemia, hypercalcemia (PTHrP), ACTH. PULM and bone metastases. Etio - most sporadic. Some vHL (chromosome 3). Tx = resection if localized. Immuno/targeted for advanced but very resistant.
Renal oncocytoma
Benign epithelial cell tumor. Large EOS w/ mitochondria w/o perinuclear clearing. Hematuria, flank pain, abdominal mass. Tx = nephrectomy
Wilms tumor
Most common renal malignancy of childhood (2-4). Embryonic glomerular. Loss of function mut’s in TSG (WT1 or WT2 on chromosome 11). OR parts of Beckwith-Wiedemann syndrome (WAGR = Wilms, Aniridia, GU map, mental Ret)
Transitional cell carcinoma
Most common tumor of urinary tract (calyces, pelvis, ureter, bladder). PAINless hematuria w/o casts -> bladder ca. Associated with Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide
Squamous cell carcinoma of the bladder
Chronic irritation leads to metaplasia then ca. RF’s = Schistosoma haematobium, chronic cystitis, smoking, chronic nephrolithiasis.
Most common acute viral cause of hemorrhagic cystitis?
Adenovirus
Acute pyelonephritis
Relative sparing of glomeruli. Etios - ascending UTI (e. coli), vesicoureteral reflux, hematogenous spread. WBC casts. CT shows striated parenchyma enhancement. Comps - chronic pyelo, renal papillary necrosis, perinephric abscess.
Chronic pyelonephritis
Recurrent episodes -> coarse, asymmetric corticomedullary scarring, blunted calyx. Path = EOSINOPHILIC casts within tubules (“thyroidization of kidney”)
Drug-induced interstitial nephritis (Tubulointerstitial nephritis)
Pyuria (eos) and azotemia occuring 1-2 weeks after drug administration (diuretics, penicillins, sulfonamides, rifampin) but MONTHS for aspirin. Pathogen - drug acts as a “hapten” - a small mol that binds to a larger one to induce a HS reaction
Acute tubular necrosis
MUDDY brown casts. Inciting event, maintenance phase (oliguric lasting 1-3 weeks w/ risk of hyperK and metabolic acidosis, death often occurs here), recovery phase (polyuric, BUN and Cr fall, risk of hypoK). Two patterns - Ischemic (dec. renal blood flow -> tubular cell death that sloughs; proximal tubule and thick ascending limb susceptible) and Nephrotoxic (toxins, crush - myoglobinuria, hemoglobinuria; proximal tubule)
FeNA in pre-renal, intrinsic, postrenal?
FeNa 2% in intrinsic. >1-2% for post-renal.
Uremia?
High BUN and Cr. Nausea, anorexia, percarditis, asterixis, encephalopathy, PLT dysfunction.
Renal failure consequences
MAD HUNGER - Metabolic Acidosis, DLD, HyperKalemia, Uremia, Na+ and water retention, Growth retardation, EPO failure -> anemia, Renal osteodystrophy
Renal osteodystrophy
Failure of Vitamin D hydroxylation -> hypoCa and hyper Phos -> secondary hyperparathyroidism. Subperiosteal thinning of bones.
ADPKD
B/l enlarged kidneys 2/2 cysts destroying parenchyma. AD - PKD1 [cell-cell adhesion] in 85% (c. 16) and PKD2 in 15% (c. 4). Associated with berry aneurysms, MV prolapse, benign hepatic cysts. Symptoms in 4th decade. Flank pain.
ARPKD
Infantile presentation. In utero -> Potter sequence. HTN, portal HTN, professive renal insufficiency.
Medullary cystic disease
Inherited. Tubulointerstitial fibrosis and renal insufficiency. US shrunken.
Simple vs. complex cysts?
Simple often outer cortex, ultra filtrate. Complex are septated, solid -> f/u +/- removal 2/2 risk of RCC.
Mannitol Use and Tox
Used for drug overdose and increased ICP. Tox - pulmonary edema, dehydration. Therefore contra’d in anuria and CHF.
Furosemide Toxicities
OH DANG - Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout
Ethacrynic acid
A loop diuretic that is NOT a sulfonamide and is therefore used for patients with sulfa drug allergy.
Diuretics that cause acidemia?
CA inhibitors. Decreased bicarb reabsorption.
Diuretics that cause alkalemia?
Loop diuretics and thiazides. Contraction alkalosis (increased ATII -> inc Na-H exchange and HCO3 reabsorption).
Diuretics that increase urine Ca?
Loop diuretics inhibit paracelular Ca reabsorption
Most common cause of hydronephrosis in utero?
Obstruction at the ereteropelvic junction (poor recanalization). Posterior urethral valve is also common. Abnormal vesicoureteral junction tends to be fairly benign with UTI’s and pyelo and ppx.
Diuretics that decrease urine Ca?
Thiazides - increased Ca+ absorption at DCT b/c inhibited Na/Cl leads to activation of Na/Ca basolateral antiporter.
Chronic renal allograft rejection mech and path?
Recipient Ab’s to graft ENDOthelium -> oblierative intimal smooth muscle hypertrophy and fibrosis of cortical arteries; the kidney gets small
Renal angiomyolipoma?
Associated with tuberous sclerosis. Benign tumor of blood vessels, smooth muscle, and fat - dx w/ CT. TS is AD w/ cortical tubers, subependymal hamartomas, sz + mental retardation, cardiac rhabdoymomas, facial angiofibromas, and leaf-shaped patches LACKING pigment.
Excretion =
Filtration + Secretion - Reabsorption
Low urine Cl- in metabolic alkalosis?
Vomiting/nasogastric tube aspiration (HCl gone) or diuretic use.
Lithium damage to kidney?
Lithium antagonizes effect of vasopressin on principal cells –> diuresis. A lithium-induced diabetes inspidus
Renal handling of urea w/ ADH?
ADH increases number of passive urea transporters in inner medullary collecting duct -> urea moves into medullary interstitium. Increases water-reabsorbing capacity of nephron (esp. at thin loop of Henle)
Collapsing gomerulopathy
HIV-associated, variant of FSGS. Includes collapse of glomerular tuft, glomerular epithelial cell hypertrophy, ATN
Meds causing hyperKalemia
Nonselective B-blockers (beta-2-mediated K uptake), ACEi, ARB, K+sparing diuretics (blocks ENaC or aldo at site of K+ excretion), NSAIDs (reduce renin and aldo secretion), Digoxin (inhibits Na/K ATPase)
High urine Cl- in metabolic alkalosis?
If hypervolemic, excess mineralocorticoid activity (Primary hyperaldo, cushing disease, ectopic ACTH), saline unresponsive. If metabolic alkalosis with high Cl- and eu or hypovolemia, consider diuretic use or Bartter and Gitelman syndromes.
How can a tumor cause diabetes insipidus?
If it produces PRHrP -> hyperCa -> renal dysf(x)
Aldosterone escape
In hyperaldosteronism, Na+ retention leads to HTN. However, compensatory rise in ANP and pressure natriuresis limits the rise in [Na+] -> HTN w/o hypernatremia (or edema). So, in hyperaldo, you see normal Na+, hypokalemia, and a metabolic alkalosis.
Clear cell renal carcinoma associated with a genetic syndrome?
VHL on chromosome 3p. Von Hippel-Lindau disease consists of cerebellar hemangioblastomas, pheochromocytomas, and clear cell renal carcinomas.
