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Estimated Renal Plasma Flow = [urine PAH] x Flow rate = PAH clearance (Underestimates RPF by 10%)
Renal Blood Flow = Renal Plasma Flow / (1-Hct)
Filtration Fraction = GFR / RPF
Filtered Load = GFR x plasma concentration
Angiotensin II Vasoconstriction (but not the afferent arteriole), Pressure Natriuresis (PCT Na absorption), Aldosterone & ADH release, thirst. Antagonized by ANP. Synthesized in liver.
Glucosuria Begins at 200mg/mL. Transport saturated @ 350mg/dL
Proximal Convoluted Tubule All Glucose, Protein, MOST Bicarb, Na, H20. Iso-osmotic
Thin Descending Loop of Henle Passive H20 absorption & urea excretion -> urine hypertonic
Thick ascending Loop of Henle NKCC pump (Where furosemide acts) actively reabsorbs salts, indirectly absorbs Mg & Ca. Impermeable to urea, H20 -> urine hypotonic
Distal Convoluted Tubule Na/Cl co-transporter (where Thiazides act). ENaC sodium reabsorption. PTH-mediated Ca reabsorption. Impermeable to urea (maintains at least some osmolarity to the hypotonic urine).
Collecting Tubules Aldosterone-mediated Na reabsorption for K. ADH mediated H20 & little urea reabsorption
PTH in the Kidney Increases PTC calcium absorption, decreases DCT PO4 absorption. Alpha1 hydroxylase expression to produce 1,25 (OH)2 Vitamin D.
Anion Gap Metabolic Acidosis Etiology PCO2<40. MUDPILES: Methanol, Uremia, DKA, Paraldehyde, Phenformin, Iron, INH, Lactic acidosis, Ethylene glycol, Salicylates
Non Anion Gap Metabolic Acidosis Etiology (8-12) PCO2<40. Diarrhea, Glue Sniffing, hyperchloremia, Renal tubular acidosis (Type 1: H pump defect, Type 2: renal bicarb loss, Type 4: Hyperaldo-> HyperK -> No ammonia excretion)
Respiratory Acidosis Etiology Hypoventilation (primary lung problem). PCO2 > 40
Respiratory Alkalosis Etiology PCO2<40. Early aspirin ingestion, Hyperventilation.
Metabolic Alkalosis Etiology PCO2>40. Diuretics, Vomiting, antacids, Hyperaldosteronism.
Metabolic Acidosis Formula 1.5(HCO3) + (6 to 10) = PCO2 (WINTER’S FORMULA)
Metabolic Alkalosis Formula .7(HCO3 increase above 40) = PCO2 increase
Respiratory Alkalosis Formula Acute: .2(PCO2 decrease) = HCO3 drop CHRONIC: .5(PCO2 decrease)= HCO3 drop
Respiratory Acidosis Formula Acute: .1(PCO2 elevation) = HCO3 increase Chronic: .35(PCO2 Elevation) = HCO3 increase
Nephritic Syndromes Type III Hypersensitivities (-Godpastures). Sx: Hematuria, HTN, Oliguria, Azotemia. Acute Post-Strep Glomerulonephritis, Membranoproliferative G., Rapidly Progressive/Crescentic G., Goodpasture’s, Berger’s/IgA Nephropathy, Alport’s.
Enlarged/hypercellular glomeruli, neutrophilic infiltrate. EM: Supepithelial humps. IF: Granular Acute Post-streptococcal Glomerulonephritis. Pediatric. Peripheral/periorbital edema. Self-resolves
Subendothelial Humps, Tram tracking (Mesangial cell consume Dense deposits & lay down new BM Membranoproliferative Glomerulonephritis. Slowly progressive to renal failure.
Crescent-Moon Shape LM & IF Rapidly progressive glomerulonephritis. Rapidly progresses to renal failure.
Linear IF. IgA mesangial deposits Berger’s Disease/ IgA Nephropathy. Mild, Post-infx. Recurrent hematuria.
Linear Immunofluorescence, Anti-GBM antibodies Goodpasture’s Syndrome (Type II hypersensitivity). Hemoptysis, hematuria.
Split basement membrane Alport’s Syndrome. Collagen Type IV mutation. Deafness, ocular disorders.
Nephrotic Syndromes Proteinuria. Frothy urine, hypoalbuminemia, peripheral & Periorbital edema, hyperlipidemia. Membranous Glomerulonephritis, Minimal Change Disease, Focal Segmental Glomerular Sclerosis (FSGS), Diabetic Nephropathy, SLE, Amyloidosis.
Diffuse capillary & BM thickening, granular immunofluorescence, spike & dome EM Membranous Glomerulonephritis. #1 in adults
Normal glomeruli & foot process effacement Minimal Change Disease #1 Pediatric. Tx: steroids
Segmental sclerosis & hyalinosis Focal Segmental Glomerular Sclerosis. HIV
K-W Nodules, BM thickening Diabetic Nephropathy
Diffuse capillary & BM thickening. Wire-loop leisions w/ subepithelial deposits SLE Nephropathy. 5 patterns.
Amyloid Deposits (Congo red +, Apple green) Amyloidosis: MM, TB, RA, chronic conditions.
Renal Cell Carcinoma Polycythemia, palpable mass, hematuria, flank pain. Associated w/ VHL (ch3), Smoking, obesity, 50-70yos. Paraneoplastic: EPO, ACTH, PTHrP, Prolactin
Wilm’s Tumor #1 Pediatric. Embryonic structures. WT1 deletion (Ch11). May be part of WAGR: Wilms, Anirida (no iris), GU malformation, MR
Transitional Cell Carcinoma #1 of Urinary tract. Painless hematuria. Associated w/Phenacetin, Smoking, Aniline dyes, Cyclophosphamide.
Pyelonephritis WBC casts pathognomonic. Affects cortex. Fever, CVA tenderness. Corticomedullary scaring, blunted calyx.
Diffuse Cortical Necrosis Abruptio Placentae, Septic shock -> DIC & Vasospasm -> Bilateral renal cortex infarction
Drug-Induced interstitial Nephritis Penicillins, NSAIDs, Diuretic-Hypersensitivity -> Interstitial Inflammation -> Systemic signs + Hematuria 2wks post-administration
Acute Tubular Necrosis #1 ARF. Ischemia/shock, Trauma, Toxins -> epithelial detachment, necrosis -> muddy brown casts. Death in early oliguric phase, recovery in 2-3 wks.
Renal Papillary Necrosis DM, Acute Pyelonephritis, Chronic Phenacetin use(ie-tylenol), Sickle Cell Anemia -> Hypoxic injury to medulla-> necrosis.
PRERENAL Acute Renal Failure High Osmolarity (>500), BUN/Cr Ratio (>20), low Na (10)& FeNa (1%) (Hypotension -> low RBF)
INTRINSIC Acute Renal Failure Low Osmolarity (<350), Moderate Na (20)& FeNa (2%), Low BUN/Cr (ATN, Ischemia, Toxins) Epithelial & Muddy Brown Casts.
POSTRENAL Acute Renal Failure Low Osmolarity (<350), high Na(40), FeNa (4%), Moderate BUN/Cr (>15). BPH, Stones, Neoplasia.
Chronic Renal Failure HTN, Diabetes Induced
Renal Failure Consequences Uremia & uremic encephalopathy. Anemia (no EPO), Renal Osteodystrophy (no VD), Hyperkalemia, Metabolic Acidosis (no excretion w/ typical high-acid diet), Na & H20 Excess (CHF & PE), Chronic Pyelonephritis, HTN
Fanconi’s Syndrome Proximal Tubule LOF -> No resorption of AAs, Glucose, PO4, Uric Acid, electrolytes. Consequences: Rickets, Osteomalacia, Hypokalemia, metabolic acidosis.
Dialysis Cysts Cortex & medulla. Due to Chronic Dialysis
Simple Cysts Cortex. Benign.
Medullary Cystic Disease Medullary. Small kidney. Poor prognosis
Medullary Sponge Disease Collecting ducts. Good prognosis.
Hyper & Hyponatremia Sx HypoNa: Disoriented, stuporous, coma. HyperNa: Irritable, Delirious, coma
High & Low Cl Etiologies Low Cl: Metabolic alkalosis, HypoK, Hypovolemia, High aldo. HIGH Cl: Non-Anion Gap Acidosis
Hyper & HypoKalmeia Sx HypoK: U waves, flat T waves, Arrhythmias, paralysis. HyperK; Peaked T waves, wide QRS, arrhythmias
Hyper & HypoCalcemia Sx HypoCa: Tetany, Neuromuscular irritability. HyperCa: Delirium, Renal Stones, Abdominal pain, +/-Calcuria
Hyper & HypoMagnesmia Sx HypoMg: Neuromuscular irritability, arrhythmias. HyperMg: Delirium, weak DTRs, cardiac arrest
Hyper & HypoPhosphatemia Sx HypoPO4: Bone loss, osteomalacia HyperPO4: Metastatic calcification, renal stones
Mannitol Mech: Osmotic diuresis. USE: Shock, drug OD, reduce ICP, IOccularP. SE: PE, dehydration, CI’d in anuria, CHF
Acetazolamide Mech: Carbonic anhydrase inhibitor, excreting HCO3. USE: Glaucoma, alkalinize urine, metabolic alkalosis, altitude sickness. SE: HyperCl metabolic acidosis, neuropathy, NH3 toxicity, Sulfa allergy
Furosemide & Ethacrynic Acid Mech: NKCC blocker, preventing urine concentration. USE: Edematous states, HTN, HyperCa. SE: Ototoxicity, HypoK, sulfa allergy, interstitial nephritis, gout.
HCTZ Mech: NaCl blocker in DCT. USE: HTN, CHF, HyperCa tx, Nephrogenic DI. SE: HypoK Metabolic Alkalosis, hypoNa; HyperGLUC: Glycemia, Lipidemia, Uricemia, Calcemia. Sulfa allergy
Spironolactone Spironolactone, Triamterene, Amiloride. Mech: Spiro: Aldosterone Receptor Blocker; Triam & Amil: CCT ENaC Blockers. Use: Hyperaldosteronism, HypoKalemia tx, CHF. SE: HyperK. Spironolactone: Gynecomastia, antiandrogenic.
ACE Inhibitors Capto, Elana,Lisino-pril. Use: HTN, CHF, Diabetic renal disease. SE: CAPTOPRIL: Cough, Angioedema, Proteinuria, Taste change, hypotension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Low angII + HyperK. CI’d in Renal Artery Stenosis
Losartan Angiotensin II Receptor Antagonist. Use: Same as ACE Inhibitors when patient has bradykinin-induced cough.
Henderson Hasselbach Equation pH= pKa + log [HCO3]/.03PCO2 Describes acid-base response
Cause of Hyperkalemia & Hypokalemia HyperK: Low insulin, aldosterone, sympathetic tone, acidosis, digitalis, hyperosmolarity. HypoK: High insulin, aldosterone or sympathetic tone, alkalosis, hypoosmolarity.
Anion gap Na - (Cl + HCO3)= anion gap
Created by: Kyle Tiemeier



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