Nephrology Flashcards

1
Q

1st trimester interim kidney - later contributes to male genital system

A

Mesonephros

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2
Q

Structures originating from ureteric bud - derived from caudal end of mesonephric duct

A

Ureter
Pelvis
Calyces
Collecting ducts

Note - Fully canalized by 10th week

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3
Q

Structures originating from interaction of metanephric mesenchyme and ureteric bud

A

Glomerulus through DCT

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4
Q

Last embryologic structure to canalize and most common site of obstruction (hydronephrosis) in a fetus

A

Ureteropelvic junction

obstruction primarily occurs in males and results in hydronephrosis because the kidney produces urine at a greater rate than can drain into the ureter

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5
Q

Kidneys trapped low in the abdomen under the inferior mesenteric artery

Associated with…
Hydronephrosis
Chromosomal aneuploidy

A

HORSESHOE KIDNEY

Inferior poles of both kidneys fuse

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6
Q

Complete absence of kidney and ureter

A

UNILATERAL RENAL AGENESIS

Ureteric bud fails to develop

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7
Q

Nonfunctional kidney consisting of cysts and connective tissue

A

MULTICYSTIC DYSPLASTIC KIDNEY

Ureteric bud fails to induce differentiation of metanephric mesenchyme

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8
Q

Y-shaped bifid ureter

Leads to…
Vesicoureteral reflux/UTIs
Ureteral obstruction

A

DUPLEX COLLECTING SYSTEM

Bifurcation of ureteric bud as it enters metanephric blastema

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9
Q

Only one functioning kidney - compensatory hypertrophy

A

CONGENITAL SOLITARY FUNCTIONING KIDNEY

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10
Q

Order of renal arteries

A
Renal artery
Segmental artery
Interlobar artery
Arcuate artery
Interlobular artery
Afferent arteriole
Glomerulus
Efferent arteriole
Vasa recta/peritubular capillaries
Venous outflow
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11
Q

Components of glomerular filtration barrier…

Size barrier
Negative charge/Size barrier
Negative charge barrier

A
Fenestrated capillary endothelium
Fused basement membrane with Heparan sulfate
Epithelial podocytes (visceral layer of Bowman's capsule)
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12
Q

Location of Juxtaglomerular cells - modified smooth muscle cells

A

Between Macula Densa (early DCT) and afferent arteriole

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13
Q

Location of ureters relative to…
Gonadal arteries
Iliac bifurcation
Uterine arteries/Vas deferens

A

Under
Over
Under

Note - Medial to gonadal vessels

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14
Q

Fluid compartments…
Total body water
ICF
ECF

A

60%
40% (includes RBC volume)
20% (includes plasma volume, interstitial fluid)

Note - All of ECF can be measured with Inulin/Mannitol, just plasma can be measured with Albumin

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15
Q

Nephrotic syndrome due to loss of which part of filtration barrier

A

Charge barrier

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16
Q

Renal Clearance (Cx) - Volume of plasma from which the substance is cleared per unit time

A

(Ux*V)/Px

Ux = Urine concentration of X
V = Urine flow rate
Px = Plasma concentration of X
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17
Q

Relationship of Cx and GFR with…
Net tubular resorption
Net tubular secretion
No tubular resorption/secretion

A

Cx < GFR
Cx > GFR
Cx = GFR (e.g. Inulin)

Note - Inulin is all filtered but not secreted, Cr is mostly filtered and somewhat secreted

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18
Q

Calculation of RBF (renal blood flow)

A

RPF/Plasma = RPF/(1-Hct)

RPF = Cpah (para-aminohippuric acid)

Note - PAH is filtered but mostly secreted (PCT) until saturation, and almost none is reabsorbed (conc. lowest in Bowman’s capsule)

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19
Q

Calculation of FF (filtration fraction)

A

GFR/RPF (normally 20%)

Note - RPF = Cpah; GFR = Ccr or Cinu

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20
Q

Effect of the following on GFR/RPF/FF…

Afferent arteriole constriction
Efferent arteriole constriction
Increased plasma protein concentration
Decreased plasma protein concentration
Ureter constriction
Dehydration
A
Decreased/Decreased/No change
Increased/Decreased/Increased
Decreased/No change/Decreased
Increased/No change/Increased
Decreased/No change/Decreased
Decreased/Decreased/Increased
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21
Q

Equation for net filtration pressure

A

(Pgc + Obs) - (Pbs + Ogc)

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22
Q

Equation for FENA

A

(Pcr x Una) / (Ucr x Pna)

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23
Q

Proximal convoluted tubule (PCT) reabsorption via Na cotransport (3) and diffusion (4)

Note - 65-80% of Na is reabsorbed in PCT in this way

Note - Isotonic resorption

A

Na cotransport:
Glucose (SGLT2/1)
Amino acids
Phosphate

Diffusion:
K
Cl-
H2O
Urea

Note - Glucose resorption is independent of insulin

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24
Q

Mechanism of NH3 secretion in proximal convoluted tubule (PCT)

A

Glutamine forms NH3 and a-ketoglutarate
a-ketoglutarate turns into bicarbonate
Bicarbonate reabsorbed from basal membrane
NH3 secreted from apical membrane

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25
Mechanism of HCO3- reabsorption in proximal convoluted tubule (PCT)
Carbonic anhydrase converts H2CO3 to CO2 and H2O CO2 resorbed Carbonic anhydrase converts CO2 and H2O to H2CO3 H2CO3 gives off H+ and resorbed from basal side as HCO3-
26
Mechanism of ATII on PCT
Stimulates Na/H+ antiporter - increases Na, H2O, and HCO3- resorption
27
Thin descending loop of Henle responsible for...
Passive reabsorbs H2O via medullary hypertonicity (impermeable to Na) - Concentrates urine (hypertonic)
28
Thick ascending loop of Henle responsible for... Note - 10-20% of Na reabsorbed here
Na, K, Cl resorption - NaK2Cl symporter Mg, Ca resorption - ROMK pumps out K to generate positive potential that drives Mg/Ca into cells Dilutes urine (impermeable to H2O; responsible for medullary hypertonicity) but individual concentrations of non-reabsorbed solutes remain the same as the amount of water remains constant
29
Early distal convoluted tubule (DCT) responsible for... Note - 5-10% of Na reabsorbed here
Na, Cl resorption - NaCl symporter Ca resorption Note - Urine most dilute here (even during water deprivation when ADH levels are high)
30
PTH action on renal tubules
Inhibits PCT apical Na/PO4- symporter decreasing PO4 resorption and thus preventing formation of insoluble calcium phosphate salts Increased TRPV5 Ca channel activity and calbindin expression levels in the distal convoluted tubule and CT Stimulates DCT basolateral Ca/Na antiporter increasing Ca resorption In PCT increases conversion of 25 Vit D to 1,25 Vit D (calcitriol) via 1a-hydroxylase
31
Collecting duct responsible for... Note - 3-5% of Na reabsorbed here
Na resorption - ENAC K secretion - ROMK H+ secretion - H+ ATPase, H/K antiporter
32
Aldosterone action on principal cells and a-intercalated cells - via mineralocorticoid receptor
Principal cells: Increased ENaC (Na resorption) Increased basolateral Na/K ATPase Increased K conductance, lumen negativity (K secretion) a-intercalated cells: Increased apical H+ ATPase activity (H secretion)
33
ADH action (2) on collecting duct in response to increased plasma osmolarity
Acts on V2 receptor to increase apical H2O channels in cortical collecting duct Increases cell surface urea transporters in medullary collecting duct to increase medullary hypertonicity and thus water resorption Note - Also acts on V1 receptor to directly increase BP
34
``` Polyuria Polydipsia Glycosuria Phosphaturia Hyperuricosuria Bicarb wasting Proteinuria/aminoaciduria Metabolic acidosis Hypophosphatemia rickets (children) Osteomalacia (adults) ```
FANCONI SYNDROME Congenital or acquired - Generalized reabsorptive defect in PCT leading to decreased resorption of amino acids, glucose, PO4, and HCO3-
35
``` Reabsorptive defect resulting in... Increased Renin Increased Aldosterone Hypokalemia Hypercalciuria Metabolic alkalosis ```
BARTTER SYNDROME Autosomal recessive defect in NaK2Cl cotransporter (thick ascending loop of Henle)
36
``` Reabsorptive defect resulting in... Increased Renin Increased Aldosterone Hypokalemia Hypocalciuria Hypomagnesemia Metabolic alkalosis ```
GITELMAN SYNDROME Autosomal recessive defect in NaCl cotransporter (DCT)
37
``` Gain of function mutation resulting in... Hypertension Decreased Renin Decreased Aldosterone Hypokalemia Metabolic alkalosis ```
LIDDLE SYNDROME Autosomal dominant gain of function mutation in collecting duct ENaC channel Treat with... Amiloride (blocks ENaC) Note - Acquired HTN with decreased Renin/Aldosterone may be SIADH
38
``` Enzyme deficiency resulting in... Hypertension Hypokalemia Metabolic alkalosis Decreased aldosterone ```
SYNDROME OF APPARENT MINERALOCORTICOID EXCESS Deficiency of 11B-hydroxysteroid dehydrogenase which converts cortisol (acts on mineralocorticoid receptor) to cortisone (inactive on mineralocorticoid receptor) Treat with... Corticosteroids to reduce endogenous cortisol production Note - Same deficiency can occur with excessive licorice consumption
39
Increased Renin secretion from JGA in response to... Note - Converts Angiotensinogen (liver) to Angiotensin I Note - Angiotensin converted to Angiotensin II in pulmonary veins
``` Decreased afferent arteriole BP Decreased Na delivery to macula densa (early DCT) Increased b1 (sympathetic) tone ```
40
Mechanism for effects of Angiotensin II... ``` Increased BP Increases FF with low RBF Increased Na reabsorption Increased H2O reabsorption Thirst Contraction alkalosis ``` Note - Prevents reflex bradycardia by acting on baroreceptors
``` AT1 receptors on vascular smooth muscle Constricts efferent arteriole Aldosterone from adrenal glands ADH from posterior pituitary Stimulates hypothalamus Increased PCT Na/H antiporter increasing HCO3 resorption ``` Note - Preferential constriction of efferent arteriole because locally produced Prostaglandins/NO at afferent arteriole counteract Angiotensin II action there
41
Action of ANP/BNP on GFR/Na reabsorption
``` Afferent arteriole dilation Efferent arteriole constriction Increased GFR and Na filtration Decreased Renin release No compensatory Na resorption in distal nephron Diuresis ```
42
Action of ATII on GFR/Na reabsorption
Efferent arteriole constriction Increased GFR and FF Compensatory Na reabsorption in proximal/distal nephron Preserves renal function (FF) while maintaining circulating volume
43
NSAIDs effect on kidney function
Block renal prostaglandin (vasodilator) production leading to afferent arteriole constriction and decreased GFR
44
Dopamine effect on kidney function
Secreted by PCT cells - dilates interlobular, afferent, and efferent arterioles increasing RBF with no change in GFR
45
``` Mechanism behind hyperkalemia caused by... Hyperosmolarity Cell death Acidosis Digitalis B-blocker Hyperglycemia/insulin deficiency ```
``` Water drags K out with it Lysis releases intracellular K Increased cellular H/K antiporter Blocks Na/K ATPase Blocks Na/K ATPase Decreases Na/K ATPase activity ``` Note - Insulin given for hyperkalemia to increase Na/K ATPase
46
``` Muscle cramps Spasms Weakness Arrhythmias EKG shows U waves with flattened T waves ```
Hypokalemia
47
Muscle weakness Arrhythmias EKG shows wide QRS with peaked T wave
Hyperkalemia
48
``` Chvostek sign (twitching) Trousseau sign (spasm) Tetany Seizures EKG shows QT prolongation ```
Hypocalcemia
49
``` Stones Bones Groans (constipation, pancreatitis) Thrones (urinary frequency) Psychiatric overtones ```
Hypercalcemia Note - Do not always see hypercalciuria
50
Tetany EKG shows Torsades Associated with hypokalemia
Hypomagnesemia
51
``` Decreased DTR Lethargy Hypotension EKG shows bradycardia Cardiac arrest Associated with hypocalcemia ```
Hypermagnesemia
52
Renal stones Metastatic calcifications Hypocalcemia
Hyperphosphatemia
53
Increased blood pressure Decreased Renin Increased Aldosterone
Primary Hyperaldosteronism (Conn Syndrome)
54
Winter's formula - predicted respiratory compensation for a metabolic acidosis
CO2 = 1.5 [HCO3] + 8 If measured CO2 is higher than calculated then suspect concomitant respiratory acidosis secondary to respiratory fatigue (e.g. DKA) If measured CO2 is lower than calculated CO2 there is a concomitant respiratory alkalosis (ASA poisoning) - Note that in this case the pH will be normal (compensation does not result in a completely normal pH)
55
MUDPILES
``` Methanol Uremia DKA Propylene glycol INH or Iron Lactic acidosis Ethylene glycol Salicylates (late) ``` Note - Early salicylate toxicity results in a respiratory alkalosis
56
Causes of normal anion gap (hyperchloremic) metabolic acidosis ("HARDASS") Note - Normal anion gap is 8-12 and is calculated by [Na]-([Cl]+[HCO3])
``` Hyperalimentation Addison's disease Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion ```
57
Hyperchloremic metabolic acidosis Hypokalemia Calcium phosphate stones Urine pH > 5.5 Caused by... Ampho B Analgesic nephropathy Congenital anomalies
DISTAL RENAL TUBULAR ACIDOSIS (TYPE 1) Defect in a-intercalated H secretion
58
Hyperchloremic metabolic acidosis Hypokalemia Hypophosphatemic rickets Urine pH < 5.5 Caused by... Fanconi syndrome Carbonic anhydrase inhibitors (Acetazolamide)
PROXIMAL RENAL TUBULAR ACIDOSIS (TYPE 2) Defect in PCT HCO3- resorption
59
Hyperchloremic metabolic acidosis Hyperkalemia Urine pH < 5.5 Caused by... Hypoaldosteronism Aldosterone resistance
HYPERKALEMIC RENAL TUBULAR ACIDOSIS (TYPE 4) Hyperkalemia results in decreased NH3 production, and thus decreased H+ excretion in the form of NH4
60
Presence of casts indicate
Glomerular or tubular origin of disease
61
Causes of RBC casts
Glomerulonephritis | Malignant HTN
62
Causes of WBC casts
Tubulointerstitial inflammation Pyelonephritis Transplant rejection
63
Causes of fatty casts (oval fat bodies) - "Maltese Cross" under polarized light
Nephrotic syndrome
64
Causes of granular (muddy brown) casts
Acute tubular necrosis
65
Causes of waxy casts
ESRD | CKD (GFR < 30)
66
Causes of hyaline casts
Normal finding - concentrated urine sample
67
``` GBM disruption resulting in... Hypertension Elevated Cr Elevated BUN (Azotemia) Oliguria Hematuria RBC casts Proteinuria < 3.5 g/d ```
NEPHRITIC SYNDROME
68
``` Podocyte/charge barrier disruption resulting in... Edema Hyperlipidemia Hypoalbuminemia Frothy urine Fatty casts Proteinuria > 3.5 g/d Hypercoagulability (ATIII loss) Increased infections (Ig loss) ```
NEPHROTIC SYNDROME Note - Aldosterone increased due to decreased effective intravascular volume (interstitial edema)
69
Causes of nephritis-nephrotic syndrome - extensive GBM damage also damages charge barrier
Diffuse proliferative glomerulonephritis | Membranoproliferative glomerulonephritis
70
``` Histology associated with... Previous skin or throat infection Hypertension Cola-colored urine Peripheral and periorbital edema Low complement (C3) High ASO/anti DNAse B titer Cryoglobulins ```
ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS LM - Hypercellular inflamed glomeruli IF - "Starry sky" granular IC deposition EM - Subepithelial humps Note - Antibiotics are to prevent Rheumatic Fever and do not treat PSGN Note - Similar finding may be seen in acute nephritic syndrome from IE
71
``` Renal histology associated with... Goodpasture syndrome Granulomatosis with polyangiitis (Wegener) Microscopic polyangiitis PSGN in adults ``` ESRD within months
RAPIDLY PROGRESSIVE (CRESCENTIC) GLOMERULONEPHRITIS LM - Crescent moon shape IF - Negative or linear pattern Note - Crescent composed of fibrin and macrophages
72
Hematuria Hemoptysis Histology showing RPGN Linear IF pattern
GOODPASTURE'S SYNDROME Type II hypersensitivity IgG against GBM type IV collagen - Cross-reaction with alveolar membranes. ``` Treat with... Emergent plasmapheresis (poor prognosis) ``` Note - Granulomatosis with polyangiitis and Microscopic polyangiitis are pauci-immune under IF
73
Histology associated with Diffuse Proliferative Glomerulonephritis (DPGN) Most common renal disease in lupus
DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS (DPGN) LM - "Wire-looping" capillaries IF - Granular IC deposition EM - Subendothelial IC deposition
74
Histology associated with... Episodic gross hematuria 2-3 days after a respiratory/GI infections Associated with Henoch-Schonlein purpura
IGA NEPHROPATHY (BERGER DISEASE) proliferation of mesangial cells, widening of the mesangium, and the glomerular endothelial proliferation LM - Hypercellular inflamed glomeruli IF - IgA-based IC deposits in mesangium EM - Mesangial IC deposition
75
Retinopathy Lens dislocation Sensorineural deafness Isolated hematuria
ALPORT SYNDROME X-linked dominant mutation in Type IV collagen Thinning and splitting of basement membrane - Basket weave on EM
76
Histology associated with Membranoproliferative Glomerulonephritis (MPGN) Type 1: Subendothelial deposits (HBV, HCV) Type 2: Deposits within basement membrane - C3 nephritic factor stabilizes C3 convertase
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS (MPGN) LM - Capillary membrane thickening with tram-tracking IF - Granular IC deposit
77
Histology associated with a child with preceding immune activation (anaphylaxis, infection) and nephrotic syndrome Associated with Hodgkin's Note - Selective albuminuria (no hypogammaglobulinemia)
MINIMAL CHANGE DISEASE LM - Normal (may see lipid) IF - Negative EM - Foot process effacement Excellent response to corticosteroids
78
Histology associated with African American or Hispanic with nephrotic syndrome Idiopathic or associated with... HIV SCD Heroin
FOCAL SEGMENTAL GLOMERULONEPHRITIS LM - Segmental hyalinosis IF - Negative EM - Foot process effacement May progress to CKD Note - If no response to steroids in minimal change disease then progression to FSGS
79
Histology associated with caucasian adult with nephrotic syndrome ``` Caused by... SLE HCV/HBV Solid tumors Drugs ```
MEMBRANOUS NEPHROPATHY LM - GBM thickening IF - Granular subepithelial IC deposition EM - "Spike and dome" May progress to CKD
80
Nephrotic syndrome with LM showing congo red stain "apple-green" birefringence under polarized light
AMYLOIDOSIS
81
Histology of diabetic nephrotic syndrome Caused by nonenzymatic glycosylation of GBM and efferent arterioles (increased GFR)
DIABETIC GLOMERULONEPHROPATHY Mesangial expansion, glomerular basement membrane thickening, and glomerular sclerosis LM - Hyaline arteriosclerosis progressing to eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesions) Note - Hyaline arteriosclerosis also seen in HTN Note - Most common cause of End Stage Renal Disease
82
Cause and treatment of kidney stone... Radiopaque on XR Radiopaque on CT Envelope/Dumbbell shaped
CALCIUM OXALATE ``` Can result from... Malabsorption (increased free Oxalate) Ethylene glycol Hypocitraturia Vit C abuse ``` Treat with... Thiazides Citrate Low-sodium diet
83
Cause and treatment of kidney stone... Radiopaque on XR Radiopaque on CT Wedge-shaped prism
CALCIUM PHOSPHATE Caused by... Increased urine pH Treat with... Thiazides
84
``` Cause and treatment of kidney stone... Radiopaque on XR Radiopaque on CT Coffin-lid Staghorn calculi ```
STRUVITE/AMMONIUM MAGNESIUM PHOSPHATE Caused by... Urease+ infection (Proteus, Klebsiella, S. saprophyticus) Treat with... Antibiotics Surgical removal of stone
85
``` Cause and treatment of kidney stone... Radiolucent on XR Minimally visible on CT Visible on US Rhomboid/Rosettes Develops slowly in acidic urine ```
URIC ACID Caused by... Gouty nephropathy Increased cell turnover/tumor lysis syndrome (e.g. Leukemia, hemolysis) Decreased urine pH (e.g. CD compensation for metabolic acidosis) Treat with... Urinary alkalinization Allopurinol
86
``` Cause and treatment of kidney stone... Radiopaque staghorn calculi on xray Sometimes visible on CT Sodium cyanide nitroprusside + (deep purple color) Hexagonal ```
CYSTINURIA Caused by... Decreased urine pH Autosomal recessive defect of renal PCT transporters (SLC3A1 gene) preventing reabsorption of Cystine, Ornithine, Lysine, and Arginine ("COLA") Treat with... Urinary alkalization and aggressive hydration is mainstay of therapy Chelating agents (e.g. Penicillamine) Low-sodium diet
87
``` Obese, smoker with... Painless hematuria Flank pain Palpable abdominal mass Fever Weight loss Polycythemia Paraneoplastic syndromes Complex cyst on US ``` Grossly golden-yellow mass Abundant clear cytoplasm with branching vascular tissue
RENAL CELL CARCINOMA Originates from PCT cells - spreads hematogenously via IVC to Lung/Bone Caused by... Autosomal dominant mutation in tumor suppressor gene VHL on Chromosome 3 - von Hippel-Lindau (hemangioblastomas, pheochromocytomas, RCC) Treat with... Resection if localized Aldesleukin (IL-2) - resistant to chemotherapy/radiation
88
Painless hematuria Flank pain Abdominal mass Grossly circumscribed mass with central scar Histologically large eosinophilic cells without perinuclear clearing
RENAL ONCOCYTOMA Benign epithelial cell tumor Treat with... Resection to rule out RCC
89
Toddler with... Large, palpable unilateral flank mass Painless hematuria
WILMS TUMOR (NEPHROBLASTOMA) Loss of function mutation mutation... WT1 mutation - Aniridia, genitourinary malformation WT2 mutation - Beckwith-Wiedemann with macroglossia, organomegaly, hemihypertrophy
90
Painless hematuria No casts ``` Associated with... Smoking Aniline dyes Cyclophosphamide Phenacetin ```
TRANSITIONAL CELL CARCINOMA OF BLADDER Note - On imaging may appear to be a kidney mass if located near renal calyces/pelvis
91
``` Painless hematuria without casts associated with... Schistosoma Chronic cystitis Smoking Chronic nephrolithiasis ```
SQUAMOUS CELL CARCINOMA OF BLADDER
92
Treatment of stress incontinence (urethral hypermobility)
Kegels Pessaries Weight loss
93
Treatment of urge incontinence (detrusor instability)
Kegels Bladder training Antimuscarinic (Oxybutynin)
94
Treatment of overflow incontinence (detrusor underactivity) Note - In DM patients lose automatic afferents (inability to sense full bladder) then autonomic efferents (inability to void)
Catheterization | a-blockers for BPH
95
Sterile pyuria and negative urine cultures
URETHRITIS Neisseria gonorrhoeae or Chlamydia trachomatis
96
Neutrophil infiltration of renal cortex with relative sparing of glomeruli and vessels
ACUTE PYELONEPHRITIS Note - On CT shows as striated parenchymal enhancement
97
Causes of... Coarse, asymmetric corticomedullary scarring Blunted calyx Eosinophilic tubular casts resembling thyroid tissue
CHRONIC PYELONEPHRITIS VUR due to perpendicular ureter insertion Chronic ureteral obstruction Posterior urethral valves in males (bilateral; malformation of Wolffian ducts results in persistent membrane) Note - If granulomatous tissue with foamy macrophages then xanthogranulomatous pyelonephritis
98
Mechanism of hypocalcemia in renal osteodystrophy - subperiosteal thinning of bones
Tubular failure means no PO4 secretion or response to PTH (hyperphosphatemia), and decreased Ca resorption Decreased calcitriol decreases intestinal Ca (and PO4) absorption Hyperphosphatemia decreases serum Ca by causing tissue calcification
99
Urine osmolality, Na, FENa, and serum BUN/Cr in prerenal azotemia
Urine osmolality > 500 Urine Na < 20 FENa < 1% BUN/Cr > 20 Note - BUN is resorbed increasing ratio
100
``` Nausea and anorexia Platelet dysfunction Pericarditis Asterixis Encephalopathy ```
UREMIA Result of consistent azotemia
101
``` Iatrogenic causes (5 Ps) of... Fever Rash CVA tenderness Hematuria Sterile pyuria with eosinophilia Elevated BUN (Azotemia) ```
ACUTE INTERSTITIAL NEPHRITIS (TUBULOINTERSTITIAL NEPHRITIS) ``` Pee (Diuretics) Pain-free (NSAIDs) Penicillins and Cephalosporins PPIs rifamPin ``` Note - Chronically presents as interstitial fibrosis and tubular atrophy (CKD)
102
``` ARF caused by... Ischemia/decreased RBF Aminoglycosides Radiocontrast Ethylene glycol Cisplatin Foscarnet Ampho B Crush injury (myoglobinuria) Hemoglobinuria ```
ACUTE TUBULAR NECROSIS Initial oliguria with recovery polyuria On histology loss of epithelial surface, vacuolar degeneration, and tubular dilation/ballooning - Preferentially affects straight proximal tubule and TALH as the medulla has low blood supply
103
``` Abrupt gross hematuria and flank pain caused by... Sickle cell disease or trait Acute pyelonephritis Renal stones within the urinary pelvis Chronic analgesic use (NSAIDs) Diabetes ```
RENAL PAPILLARY NECROSIS Note - Coagulation necrosis with preserved tubule outline
104
``` Adult with... Hypertension Bilateral flank pain Hematuria Urinary infections Progressive renal failure ``` Associated with... Berry aneurysms Benign hepatic cysts MVP Note - Cysts are non-enhancing on CT
AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE Mutation in PKD1 on Chromosome 16 and PKD2 is on chromosome 4
105
``` Child with... Potter sequence Oliguria Hypertension Portal hypertension Progressive renal failure ``` Associated with... Congenital hepatic fibrosis
AUTOSOMAL RECESSIVE POLYCYSTIC KIDNEY DISEASE Cystic dilation of collecting ducts
106
Effect of hydronephrosis on GFR and FF
Buildup of backpressure into Bowman's space causes reduced GFR which decreases FF
107
Region of nephron responsible for majority of water resorption
PCT (even in dehydrated state) Note - While PCT reabsorbs the most water, the late DCT and Collecting Duct are responsible for increased reabsorption in dehydration
108
Which rib can penetrate the kidneys
12th Note - 9th - 11th may damage the spleen or liver instead
109
``` Fever Neurologic symptoms Renal failure Anemia with schistocytes Thrombocytopenia ``` Prolonged bleeding time Normal PT and aPTT
THROMBOCYTOPENIC THROMBOTIC PURPURA (TTP) Platelet activation in arterioles and capillaries, diffuse microvascular thrombosis, and microangiopathic hemolytic anemia Note - Other thrombotic microangiopathy (HUS) does not commonly present with neurologic symptoms
110
Excretion Rate equation
Filtration rate - Reabsorption rate (GFR x P) - Reabsorption rate Note - Secretion rate = Excretion rate - Filtered rate
111
``` Mechanism of ARF caused by... Sulfonamides Methotrexate IV Acyclovir Triameterene ```
Precipitation and tubular obstruction Note - Amorphous hyaline tubular obstruction might be Tamm-Horsfall proteins from Multiple Myeloma
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Mechanism of cystitis Note - No fever or flank pain
Suppression of endogenous flora allows for colonization by pathogenic GNRs Note - Anatomic abnormalities (e.g. VUR due to repeated cystitis) required for pyelo
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Straw-colored discharge from umbilicus with surrounding erythema
PATENT URACHUS/ALLANTOIC DUCT (URACHAL FISTULA) Normally obliteration forms the median umbilical ligament (medial is distal umbilical artery) which connects the upper end of the bladder to the umbilicus Note - Only patent distal urachus forms sinus (purulent discharge), while only patent proximal urachus forms urachal cyst
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Management of patient with microalbuminuria (< 300 mg/d) Note - Not detected by normal urine dipstick
ACEi Note - Initially before microalbuminuria glomerular hypertrophy causes hyperfiltration and elevated GFR
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Mechanism of hyperkalemia in DKA
Osmotic diuresis from ketones High serum osmolarity increases Aldosterone Aldosterone increases K loss Increased serum osmolarity and H Drives K out and H in ECF hyperkalemia with ICF hypokalemia
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Effect on ECF, ICF, and Osmolarity by... ``` DI, Sweating, Dehydration Hemorrhage, Diarrhea Adrenal insufficiency Hypertonic saline Polydipsia, SIADH ```
Hyperosmotic volume contraction (ECF, ICF) Isosmotic volume contraction (ECF) Hypoosmotic ECF contraction and ICF expansion Hyperosmotic ECF expansion and ICF contraction Hypoosmotic ECF euvolemia and ICF expansion
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Newborn with... Absence of normal pelvicalyceal system Ureteral atresia
MULTICYSTIC KIDNEY DYSPLASIA
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Metabolic alkalosis with... Low urine chloride High urine chloride
Low: Vomiting (saline-responsive) Prior diuretic use (saline-responsive) High: Current diuretic use (saline-responsive) Bartter/Gitelman (saline-unresponsive) Hyperaldosteronism/Cushing's (saline-unresponsive)
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Most common cause of death in patients with CKD
CAD
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Mechanism of decreased BUN/Cr in intrinsic ARF
Debris obstructs tubules and prevents resorption of H2O, Na, and Urea - Decreased urinary osmolality, increased urinary Na/FENA, and decreased BUN/Cr
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High cell turnover treated with chemotherapy prevent with urine alkalinization and hydration DCT and collecting ducts
tumor lysis syndrome causing Na, K, uric acid release into serum uric acid ppt in acidic environment of DCT and collecting ducts
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desmopressin administration effects on someone with DI
increase ADH increased V2 receptor mediated increase in water reabs activates urea transporters to increase urea reabs and thus also water reabs gradient
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How is renal blood flow maintained at a near constant level as SBP increases
Via RBF autoregulation through reflexive constriction of the afferent arterioles in response to rising arterial pressure rapid component: myogenic mechanism ( vascular smooth mm cells contract reflexively in response to rising wall tension caused by increasing perfusion pressure) follow by Slower component: Tubuloglomerular feedback (TGF is when SBP rises the GFR rises also which increases NaCl delivery to macula densa. This causes MD to release ATP and adenosine which diffuse via mesangial cells to the afferent arteriole where they stimulate contraction) NOTE: efferent arteriole does not contribute to autoregulation of renal blood flow
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What is the renal threshold for glucose? | What happens to the threshold with chronic hyperglycemia?
180-200 mg/dl plasma glucose levels above this range cause glucosuria (glucose reabsorption is carrier mediated. There is saturation of renal Na-glucose cotransport capacity) Chronic hyperglycemia (diabetes) can raise the renal threshold
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Glucose reabsorption pathway
- glucose is freely filtered across the glomerular filtration barrier and normally 100% is reabsorbed in the proximal tubule - proximal tubule reabsorption is via SGLT2 (low affinity, high capacity) and SGLT1 (high affinity, low capacity) Na-glucose cotransporters - the transport maximum (Tm) is reached when all glucose carriers in all nephrons are saturated
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how does GFR affect the transport maximum
Increase GFR, lowers the threshold decrease GFR, increases the threshold why? increasing GFR increases the glucose filtered load and renal transport capacity is rapidly overwhelmed causing glucosuria even though plasma concentration was not changed
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this diuretic increases the risk of hypercalcemia what is the mechanism
Thiazides inhibit NaCl reabsorption but also enhance reabsorption of calcium via TRPV5 Ca channel "ca sparing diuretics" at the distal convoluted tubule
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HTN with increased plasma renin activity but normal aldosterone/renin ratio. What is causing the increased plasma renin
increased sympathetic nervous system activity is a contributing factor in many cases of essential hypertension. This increases renin secretion via B1 adrenergic receptors which then causes angiotensin II and aldosterone to rise.
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When is acetazolamide contraindicated and why
patients with hypokalemia, hyponatremia, metabolic acidotic states (non-anion gap), and severe hepatic/renal dysfunction it causes acidosis because it inhibits CA which is associated with rapid increase in urinary HCO3 excretion --> alkaline urine --> metabolic acidosis
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Generalized aminoaciduria and more specific abnormalities of tryptophan metabolism
Hartnup disease
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Septic patient that develops purpura and ecchymoses over the trunk and legs. Develops anuria (unable to pass urine) and causes uremic death What do you expect to see on renal autopsy? labs show low platelets, low fibrinogen, increased PT and PTT (due to consumption of clotting factors), and presence of fibrin degradation products.
Diffuse Cortical Necrosis This pt has disseminated intravascular coagulation as a complication of gram negative sepsis. Widespread clotting and fibrinolysis occurs producing thrombosis in many renal vessels and causing diminished vascular perfusion, leading to diffuse cortical necrosis
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Cortical scarring or benign nephrosclerosis is a chronic change seen with
diabetes mellitus type 2 and hypertension there is hyaline arteriolosclerosis, glomerulosclerosis, tubular atrophy, and interstitial fibrosis
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Wedge shaped necrosis
focal and seen in acute renal infarct due to trauma, thrombus, or embolus
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Mechanism causing sickle cell nephropathy
sickling crisis occurs within areas of high osmolarity, hypoxia, and slow blood flow rates of the vasa recta of the renal medulla (renal medulla has very high osmolarity and is a hypoxic environment) sickling within the vasa recta can lead to patchy papillary necrosis, hematuria, proteinuria, and sometimes renal scarring
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complications associated with rapid correction of sodium: 1) high to low 2) low to high
1) high to low. The brain will blow 2) low to high. The pons will die (osmotic demyelination syndrome affecting the corticospinal and corticobulbar areas in basis pontis) and can cause "locked in" syndrome (vertical eye movements and blinking remain intact)
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Calculating amount of sodium reabsorbed by the renal tubule each day
Na reabsorbed=filtered-excreted filtered= GFR x plasma sodium concentration Excreted=urinary Na concentration x urinary flow note: GFR=inulin or creatinine clearance
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Increased BUN and creatinine suggests
decreased GFR
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virulence factor of proteus mirabilis causing staghorn calculi tx with fluoroquinolones
urease raises the pH of the urine by splitting urea and forming ammonia in the presence of ammonia, the magnesium ammonium phosphate(struvite) is produced and causes the formation fo the staghorn renal calculi
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Patient presents with damage to base of the skull and now have low specific gravity in his urine
Central diabetes insipidus This type of fracture is associated with damaged hypothalamus or pituitary gland resulting in an inability to make vasopressin in the hypothalamus and store in the pituitary gland
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ACE inhibitors are often used in patients with early stage chronic kidney disease because it has reno-protective effects (decreased glomerular load and protein filtration). In what situation would you NOT give ACE inhibitors
atherosclerotic renal artery stenosis (renal artery bruit and history of atherosclerotic cardiac disease) Means there is baseline renal hypoperfusion. Adding ACE inhibitor decreases GFR durthere and patient can develop acute kidney injury with elevated creatinine avoid in settings of hypoperfusion (shock etc.)
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Patient has a severe flank pain radiating to the groin with intermittent hematuria. You do a high resolution CT
Ureteral obstruction from renal stone CT will show stone or ureteral dilation
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How does hyperglycemia cause ADH resistance
1) hyperglycemia increases glucose delivery to the proximal tubule and exceeds its re-absorptive capacity, causing osmotic diuresis 2) high volume flow through the renal tubule washes out the corticopapillary osmotic gradient established by the loop of henle 3) This gradient is required for reabsorption of water from the collecting duct, so hyperglycemia can cause ADH resistance
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Poorly managed type 2 DM is most likely to produce a
hyperglycemic, hyperosmotic, non-ketotic state (HHNS) hypernatremia high chloride hypokalemia
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common complication of urinary tract stones
acute pyelonephritis due to microtraumatic injuries to the mucosa and urine stasis facilitating bacterial proliferation
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why does increasing hematocrit cause a increase in renal blood flow
Hematocrit represents the percentage of blood volume occupied by RBCs increases hct will decrease plasma volume and increase glomerular capillary oncotic pressure this opposes filtration, so RBF increase to ensure the glomerular filtration rate is maintained at an optimal level
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Diuretics lead to aldosterone excess and hypokalemia by the following mechanisms:
1) diuretic induced volume depletion causing increase in angiotensin II and stimulation of potassium excretion 2) saline diuresis increases sodium delivery to the distal segments 3) saline diuresis also causes rapid fluid flow in the distal segments which prevents potassium reabsorption
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Renal complication of aortic dissection
bilateral renal infarction dissection progresses distally to involve the major arteries arising from the aorta. This can cause bilateral renal artery occlusion, leading to renal hypoperfusion and infarction with flank pain and hematuria.
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Produces a positive dipstick test for blood without hemoglobin/rbc in microscopic examination
myoglobinuria dipstick test detects peroxidase activity rather than specifically reacting to blood. hydration and alkalinization of the urine is essential to prevent renal damage due to precipitation of myoglobin in the tubules, which causes obstruction and generation of reactive oxygen species
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HSN reaction for lupus nephritis and IF pattern
granular lumpy bumpy pattern due to random deposition of immune complexes into the glomerular basement membrane type III HSN)