USMLE - Renal Part 2 | Flashcards Deck

What ions does Aldosterone affect?

Increased reabsorption of Na

| Increased secretion of K and H

What shifts K out of cells (HyperK)?

DO Insulin LAB

| Digitalis, HyperOsmolarity, Insulin deficiency, Lysis of cells, Acidosis, Beta Antagonists

What shifts K into cells (HypoK)?

"Insulin shifts K into cells"

| Hypo-osmolarity, Insulin, Alkalosis, Beta agonists

Low [Na] presents with:

Nausea, Malaise, Stupor, Coma

High [Na] presents as

Irritability, stupor, coma

Low [K] presents as

U wave, Flat T wave, Arrhythmias, muscle weakness

High [K] presents as

Wide QRS and peaked T waves, Arrhythmias, muscle weakness

Low [Ca] presents as

Tetany, seizures

High [Ca] presents as

Stones (renal stones), Bones (pain), Groans (abdominal pain), Psychiatric overtones (anxiety, altered mental status), but not necessarily calcinuri...

Low [Mg] presents as

Tetany, arrhythmias

High [Mg] presents as

"Lazy DR. Better Hike/Cram Ca"

| Lethargy, decreased deep tendon reflexes, bradycardia, hypotension, cardiac arrest, hypocalcemia

Low [PO4] presents as

Bone loss, osteomalacia

High [PO4] presents as

Renal stones, metastatic calcifications, hypocalcemia

Metabolic Acidosis: pH, PCO2, [HCO3], Compensatory response?

Low pH, Low PCO2, Low [HCO3], Immediate hyperventilation

Metabolic Alkalosis: pH, PCO2, [HCO3], Compensatory response?

High pH, High PCO2, High [HCO3], Immediate hypoventilation

Respiratory Acidosis: pH, PCO2, [HCO3], Compensatory response?

Low pH, High PCO2, High [HCO3], Delayed increase in bicarb reabsorption

Respiratory Alkalosis: pH, PCO2, [HCO3], Compensatory response?

High pH, Low PCO2, Low [HCO3], Decreased renal bicarb reabsorption

Kidney Henderson-Hasselbalch Equation for Kidney

pH = 6.1 + log ([HCO3]/.(.03 x PCO2))

How does one predict the compensation for a simple Met Acidosis? What if actual PCO2 is different from predicted?

Winters Formula: PCO2 = (1.5 x [Bicarb]) + 8) +/- 2

| If not as predicted: Mixed acid/base disorder

Anion Gap Calculation

| Normal Anion Gap?

Na - (Cl + HCO3)

| Normally 8-12 mEq/L

Causes of Resp Acidosis?

Hypoventilation due to Obstruction, Disease, Opioids or Sedatives, Muscle weakness

Causes of Anion Gap Met Acidosis

MUDPILES

Methanol (formic acid), Uremia, Diabetic ketoacidosis, Propylene glycol, Iron tablets or INH, Lactic acidosis, Ethylene glycol (Oxal...

Causes of Non Anion Gap Met Acidosis

HARD ASS

| Hyperalimentation, Addisons Disease, Renal Tubular Acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion

Causes of Resp Alkalosis?

Hyperventilation (i.e. altitude sickness)

| Salicylates (early)

Causes of Met Alkalosis?

Loop Diuretics, Vomiting, Antaacids, Hyperaldosteronism

Type 1 Renal Tubular Acidosis

Location of defect

Defect

Urine pH

Associated with

Increased risk for

Defect in DT ability to excrete H
Urine pH > 5.5
Associated with HypoK
Increased risk for CaPO4 kidney stones because of increased urin...

Type 2 Renal Tubular Acidosis

Defect in

Defect

Seen in what disease?

Urine pH

Associated with

Increased risk for

Defect in PT HCO3 reabsorption

Seen in Fanconi Syndrome

Urine pH < 5.5

Associated with hypoK

Increased risk for hypophos...

Mechanism of Type 4 Renal Tubular Acidosis

Low Aldosterone or lack of response to aldosterone --> hyperK --> impaired ammoniagenesis in PT --> PT loses buffering capacity --> uri...

What do Casts in Urine indicate?

Renal (vs. Bladder) origin

RBC Casts Indicate

Glomerulonephritis, Ischemia, MalHTN

WBC Casts indicate

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

Fatty Casts
Appearance
Indication

Oval Fat Bodies

| Indicate Nephrotic Syndrome

Granular (Muddy Brown) Casts Indicate

ATN

Waxy Casts indicate

Advanced renal disease, Chronic renal failure

Hyaline casts indicate

Non-specific. Can be a normal finding

Causes of hematuria without casts

Bladder Cancer or Kidney Stones

Causes of pyuria without casts

Acute Cystitis

Definition of Focal Glomerular Disorder

<50% glomeruli involved

Definition of Diffuse Glomerular Disorder

50% glomeruli involved

Definition of Proliferative Glomerular Disorder

Hypercellular glomeruli

Definition of Membranous Glomerular Disorder

Thickening of glomerular BM

Definition of Primary Glomerular Disorder

Only glomeruli involved

Definition of Secondary Glomerular Disorder

Glomeruli + other organ involved

Names of Nephritic Syndromes

"PARIS"
PSGN, RPGN, Berger's IgA Glomerulonephrtopathy, Alport Syndrome
(DPGN and MPGN can also be nephrotic)
(SLE can also cause a nephri...

Names of Nephrotic Syndromes

"F. SAM M.D."
Focal Segmenting Glomerulosclerosis, Amyloidosis, SLE, Membranous Nephropathy, Minimal Change Disease, Diabetic Glomerulonephropat...

Presentation of Nephrotic Syndrome
Casts
Associated with
Increased risk for

"Protein LEACHs out"
Proteinuria > 3.5 g/day, ↑Lipids, Edema, hypoAlbuminia, ↑Cholesterol, HTN (Na retention)
Fatty Casts
Associated wi...

FSGS

LM

EM

Rate

Associated with diseases? drug use? lifestyle? medicines?

LM: segmental sclerosis and hyalinosis
EM: effacement of foot processes
Most common nephrotic syndrome in adults
Associated with HIV, Hero...

Membranous Nephropathy

Mechanism

LM

EM

IF

What diseases present this way?

Rate

Caused by

"MP"

Subepithelial IC deposition

LM: Diffuse capillary and BM thickening

EM: "Spike and Dome" with subepithelial deposits

Amyloidosis
LM
Associated with…

LM: congo red stain shows apple-green birefringence under polarized light
Associated with chronic conditions like Multiple Myeloma, TB, and RA

Related Flashcard Decks

Microbiology

USMLE - Micro AntiMicrobials

These antibiotics — Penicillin, Methicillin, Ampicillin, Piperacillin, Cephalosporins, Aztreonam, and Imipenem — prevent bacterial cell wall formation by inhibiting peptidoglycan cross-linking, leading to cell lysis and death.

81 cards

View Deck

Microbiology

USMLE - Micro Systems

The skin’s normal dominant flora is Staphylococcus epidermidis, a non-pathogenic bacterium that helps protect against harmful microbes by competing for space and nutrients.

113 cards

View Deck

Microbiology

USMLE - Micro Viruses

Reassortment occurs when viruses with segmented genomes exchange genetic segments, creating new combinations. This can lead to rapid evolution, high-frequency recombination, and potentially global pandemics. A common example is the influenza virus.

123 cards

View Deck

Microbiology

USMLE - Micro Parasites

The movement of molecules against their concentration gradient, from low to high concentration, using energy from ATP.

40 cards

View Deck

Microbiology

USMLE - Micro Mycology

Includes Histoplasma, Blastomyces, Coccidioides, and Paracoccidioides, which cause pneumonia and systemic dissemination

13 cards

View Deck

Microbiology

USMLE - Micro Bacteria

Identification begins with the catalase test: catalase-negative indicates Streptococcus, catalase-positive indicates Staphylococcus. Staph aureus is coagulase-positive, while S. epidermidis (novobiocin-sensitive) and S. saprophyticus (novobiocin-resistant) are coagulase-negative.

117 cards

View Deck

Microbiology

USMLE - Micro Basic

Peptidoglycans are composed of a sugar backbone (N-acetylglucosamine and N-acetylmuramic acid) with peptide side chains cross-linked by transpeptidase. They provide structural support and protect bacteria from osmotic lysis.

71 cards

View Deck

Microbiology

USMLE - Reproduction Part 4

Cryptorchidism is the failure of one or both testes to descend into the scrotum, often seen in premature infants. It leads to impaired spermatogenesis due to higher abdominal temperatures but usually normal testosterone if unilateral. It is associated with an increased risk of germ cell tumors, and labs may show ↑ FSH, ↑ LH, ↓ inhibin B, and ↓ testosterone if bilateral.

16 cards

View Deck

Microbiology

USMLE - Reproduction Part 3

Male genital development is initiated by the SRY gene, which produces testes-determining factor, leading to testis formation. Sertoli cells secrete Müllerian Inhibitory Factor (MIF) to suppress female duct development, while Leydig cells produce testosterone, promoting the development of mesonephric (Wolffian) ducts into male internal genitalia.

100 cards

View Deck

USMLE - Renal Part 2

Term	Definition
What ions does Aldosterone affect?	Increased reabsorption of Na \| Increased secretion of K and H
What shifts K out of cells (HyperK)?	DO Insulin LAB \| Digitalis, HyperOsmolarity, Insulin deficiency, Lysis of cells, Acidosis, Beta Antagonists
What shifts K into cells (HypoK)?	"Insulin shifts K into cells" \| Hypo-osmolarity, Insulin, Alkalosis, Beta agonists
Low [Na] presents with:	Nausea, Malaise, Stupor, Coma
High [Na] presents as	Irritability, stupor, coma
Low [K] presents as	U wave, Flat T wave, Arrhythmias, muscle weakness
High [K] presents as	Wide QRS and peaked T waves, Arrhythmias, muscle weakness
Low [Ca] presents as	Tetany, seizures
High [Ca] presents as	Stones (renal stones), Bones (pain), Groans (abdominal pain), Psychiatric overtones (anxiety, altered mental status), but not necessarily calcinuria
Low [Mg] presents as	Tetany, arrhythmias
High [Mg] presents as	"Lazy DR. Better Hike/Cram Ca" \| Lethargy, decreased deep tendon reflexes, bradycardia, hypotension, cardiac arrest, hypocalcemia
Low [PO4] presents as	Bone loss, osteomalacia
High [PO4] presents as	Renal stones, metastatic calcifications, hypocalcemia
Metabolic Acidosis: pH, PCO2, [HCO3], Compensatory response?	Low pH, Low PCO2, Low [HCO3], Immediate hyperventilation
Metabolic Alkalosis: pH, PCO2, [HCO3], Compensatory response?	High pH, High PCO2, High [HCO3], Immediate hypoventilation
Respiratory Acidosis: pH, PCO2, [HCO3], Compensatory response?	Low pH, High PCO2, High [HCO3], Delayed increase in bicarb reabsorption
Respiratory Alkalosis: pH, PCO2, [HCO3], Compensatory response?	High pH, Low PCO2, Low [HCO3], Decreased renal bicarb reabsorption
Kidney Henderson-Hasselbalch Equation for Kidney	pH = 6.1 + log ([HCO3]/.(.03 x PCO2))
How does one predict the compensation for a simple Met Acidosis? What if actual PCO2 is different from predicted?	Winters Formula: PCO2 = (1.5 x [Bicarb]) + 8) +/- 2 \| If not as predicted: Mixed acid/base disorder
Anion Gap Calculation \| Normal Anion Gap?	Na - (Cl + HCO3) \| Normally 8-12 mEq/L
Causes of Resp Acidosis?	Hypoventilation due to Obstruction, Disease, Opioids or Sedatives, Muscle weakness
Causes of Anion Gap Met Acidosis	MUDPILES Methanol (formic acid), Uremia, Diabetic ketoacidosis, Propylene glycol, Iron tablets or INH, Lactic acidosis, Ethylene glycol (Oxalic Acid), Salicylates (late)
Causes of Non Anion Gap Met Acidosis	HARD ASS \| Hyperalimentation, Addisons Disease, Renal Tubular Acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion
Causes of Resp Alkalosis?	Hyperventilation (i.e. altitude sickness) \| Salicylates (early)
Causes of Met Alkalosis?	Loop Diuretics, Vomiting, Antaacids, Hyperaldosteronism
Type 1 Renal Tubular Acidosis Location of defect Defect Urine pH Associated with Increased risk for	Defect in DT ability to excrete H Urine pH > 5.5 Associated with HypoK Increased risk for CaPO4 kidney stones because of increased urine pH and bone resorption
Type 2 Renal Tubular Acidosis Defect in Defect Seen in what disease? Urine pH Associated with Increased risk for	Defect in PT HCO3 reabsorption Seen in Fanconi Syndrome Urine pH < 5.5 Associated with hypoK Increased risk for hypophosphatemic rickets
Mechanism of Type 4 Renal Tubular Acidosis	Low Aldosterone or lack of response to aldosterone --> hyperK --> impaired ammoniagenesis in PT --> PT loses buffering capacity --> urine pH decreases
What do Casts in Urine indicate?	Renal (vs. Bladder) origin
RBC Casts Indicate	Glomerulonephritis, Ischemia, MalHTN
WBC Casts indicate	Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
Fatty Casts Appearance Indication	Oval Fat Bodies \| Indicate Nephrotic Syndrome
Granular (Muddy Brown) Casts Indicate	ATN
Waxy Casts indicate	Advanced renal disease, Chronic renal failure
Hyaline casts indicate	Non-specific. Can be a normal finding
Causes of hematuria without casts	Bladder Cancer or Kidney Stones
Causes of pyuria without casts	Acute Cystitis
Definition of Focal Glomerular Disorder	<50% glomeruli involved
Definition of Diffuse Glomerular Disorder	50% glomeruli involved
Definition of Proliferative Glomerular Disorder	Hypercellular glomeruli
Definition of Membranous Glomerular Disorder	Thickening of glomerular BM
Definition of Primary Glomerular Disorder	Only glomeruli involved
Definition of Secondary Glomerular Disorder	Glomeruli + other organ involved
Names of Nephritic Syndromes	"PARIS" PSGN, RPGN, Berger's IgA Glomerulonephrtopathy, Alport Syndrome (DPGN and MPGN can also be nephrotic) (SLE can also cause a nephritic syndrome) "PIG ARMS" includes Goodpastures and MPGN
Names of Nephrotic Syndromes	"F. SAM M.D." Focal Segmenting Glomerulosclerosis, Amyloidosis, SLE, Membranous Nephropathy, Minimal Change Disease, Diabetic Glomerulonephropathy (DPGN and MPGN can also be nephritic)
Presentation of Nephrotic Syndrome Casts Associated with Increased risk for	"Protein LEACHs out" Proteinuria > 3.5 g/day, ↑Lipids, Edema, hypoAlbuminia, ↑Cholesterol, HTN (Na retention) Fatty Casts Associated with Thromboembolism (hypercoagulable state due to ATIII loss) Increased risk for infection (from loss of gamma Igs)
FSGS LM EM Rate Associated with diseases? drug use? lifestyle? medicines?	LM: segmental sclerosis and hyalinosis EM: effacement of foot processes Most common nephrotic syndrome in adults Associated with HIV, Heroin, Obesity, Interferon treatment, Chronic kidney disease (due to congenital absence or removal)
Membranous Nephropathy Mechanism LM EM IF What diseases present this way? Rate Caused by	"MP" Subepithelial IC deposition LM: Diffuse capillary and BM thickening EM: "Spike and Dome" with subepithelial deposits IF: Granular (IgG and C3) SLE's presentation 2nd most common Nephrotic in adults Causes: idiopathic, drugs, infections, SLE, tumors
Minimal Change Disease Pathogenesis LM EM Describe the Proteinuria Triggered by Most common in Treatment	T Cell Cytokines LM: normal EM: foot process effacement Selective loss of albumin, not globins, because of BM polyanion loss Triggered by recent infection or immune stimulus Most common in children Responds to corticosteroids
Amyloidosis LM Associated with…	LM: congo red stain shows apple-green birefringence under polarized light Associated with chronic conditions like Multiple Myeloma, TB, and RA
MPGN Type I Mechanism IF Appearance Associated with	Subendothelial IC deposits IF: Granular Tram-Track appearance due to BM splitting caused by mesangial ingrowth HBV, HCV
MPGN Type II Mechanism Appearance Associated with	Intramembranous IC deposits AutoAb --/ degradation of C3 convertase which leads to low levels of C3 "Dense deposits" Associated with C3 nephritic factor
Diabetic Glomerulonephropathy \| Mechanism	Nonenzymatic Glycosylation of BM --> ↑ permeability to proteins + ↑ thickness NEG of EA --> hyaline arteriolosclerosis --> ↑GFR --> hyperfiltration --> damage to mesangial cells --> mesagnial expansion Osmotic damage to glomerular capillary endothelial cells (Glucose --> sorbitol which is osmotically active and leads to swelling and cellular damage)
ATII receptor MoA	ATIIR --> IP3 \| ATIIR --/ cAMP
In Nephrotic Syndrome, what is the glomerular injury due to?	Cytokines damage podocytes causing them to fuse and destroy - charge of GBM
Which diabetes causes Diabetic Glomerulonephropathy?	Both. 1 (40%) > 2 (20%)
Diabetic Glomerulonephropathy \| LM	LM: Mesangial expansion, BM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson Lesion)
Nephritic Syndrome What kind of process? What is it mediated by?	Inflammatory Process mediated by neutrophils
Nephritic Syndrome Presentation	"PR HOZ" Proteinuria (<3.5g/day) RBC casts Hematuria, HTN (due to salt retention) Oliguria aZotemia
PSGN Presentation Treatment	"Throat, Bloat, Coke" Child w/ previous infection (GAS), peripheral + periorbital edema, HTN, and dark urine Resolves Spontaneously
PSGN LM EM IF	LM: Glomeruli enlarged and hypercellular. Neutrophils, "lumpy bumpy" EM: Subepithelial IC humps IF: Granular appearance due to IgG, IgM and C3 deposition along BM and mesangium
RPGN (crescentic) LM IF What are in the crescents?	LM + IF: crescent moon shape \| Crescents = fibrin + plasma proteins (C3) with glomerular parietal cells, monocytes, and macs
RPGN prognosis	Poor (days to weeks)
Diseases that result in RPGN \| Markers for them?	Goodpasture's (hematuria + hemoptysis), Wegener's (cANCA), Microscopic polyangiitis (pANCA)
How Goodpasture's --> RPGN What kind of Rxn? Mechanism	Type II Hypersensitivity Rxn \| Abs to GBM + alveolar BM
Goodpasture's IF	Linear pattern
DPGN Mechanism What diseases cause it? LM EM IF	Subendothelial IC mediated SLE + MPGN cause it LM: wire looping of capillaries EM: subendothelial and sometimes intramembranous IgG-based IC often with C3 deposition IF: granular
Most common cause of death in SLE	DPGN
Which diseases can cause concurrent nephrotic and nephritic syndromes?	SLE and MPGN
Berger's Disease (IgA Nephropathy) Related to what other disease? LM EM IF	"AM" Think Mesangium Related to Henoch-Schonlein Purpura LM: mesangial proliferation EM: mesangial IC deposits IF: IgA based IC deposits in mesangium
When does Berger's disease often presents/flares?	Often presents/flares with URI or acute gastroenteritis
Henoch-Schonlein Purpura Kind of vasculitis? Most common vasculitis in... Classic Presentation Disease Mediated by Associated with Age of lesions?	Small vessels Most common vasculitis in children "NAPA" Child following URI with Nephropathy, Abdominal pain (melena), Purpura, Arthralgia Mediated by IgA complex deposition Associated with IgA nephropathy Multiple lesions of same age
Wegener's Granulomatosis (Granulomatosis with Polyangiitis) Kind of vasculitis? Presentation Histo Blood CXR Treatment	Small vessels Upper Respiratory Tract: Perforated nasal septum, sinusitis, otitis media, mastoiditis Lower RT: Hemoptysis, Cough, Dyspnea Renal: Hematuria, RBC Casts Focal Necrotizing vasculitis + Necrotizing granulomas in the lung and upper airway + Necrotizing glomerulonephritis c-ANCA Large Nodular Densities Cyclophosphamide and corticosteroids
Alport Syndrome Mechanism Genetics Presentation	"Imagine the V in IV splitting the BM" Mutation in IV collagen --> split basement membrane X linked Glomerulonephritis, deafness, eye problems
Treat and prevent Kidney Stones with	Fluid intake
Ca Kidney Stones Frequency Precipitates at what pH XR	80% CaPO4 --> ↑pH CaOxalate --> ↓pH Radiopaque
Oxalate crystals can result from	Ethylene glycol or VitC abuse
Treatment for recurrent kidney stones	Thiazide and citrate
Most common kidney stone presentation Re: Kind of Kidney stone, Urine, and Blood?	CaOxalate stone in pt with hypercalcinuria and normocalcemia
Ammonium MgPhosphate Kidney Stones (struvite) Frequency Precipitates at pH XR	15% Precipitates at ↑pH Radiopaque
Ammonium MgPhasphate Kidney Stones Caused by Mechanism What can they form?	Caused by infection with urease+ bugs (proteus mirabilis, Staph, Klebsiella) The bugs hydrolyze urea to ammonia and this alkalizes urine Can form staghorn calculi that can be a nidus for UTIs
Uric Acid Kidney Stones Frequency Precipitates at pH XR	5% Precipitates at ↓pH RadiolUcent
Uric Acid Kidney Stones Visible on Associated with Often seen in what kind of diseases? Treatment	Visible on CT and US but not XR Associated with hyperuricemia (gout) Often seen in diseases with high cellular turnover (leukemia) Treat w/ alkalinization of urine
Cystine Kidney Stones Frequency Precipitates at pH XR Usually Secondary to Appearance of stone Treatment	Cystine Kidney Stones Frequency Precipitates at pH XR Usually Secondary to Appearance of stone Treatment
Hydronephrosis What happens? Can be caused by Leads to May result in	Backup of urine into the kidney Caused by urinary tract obstruction or vesicoureteral reflux Leads to dilation of renal pelvis and calyces Results in parenchymal thinning
ATN Frequency? Reversible? When does death most frequently occur?	Most common cause of intrinsic renal failure Self reversible in some cases but can be fatal if untreated Death most often occurs during oliguric phase
ATN \| What causes it?	Renal ischemia (from shock, sepsis) Crush injury (myogloniburia) Drugs, toxins
Acute Tubular Necrosis Stages	Initiation: Ischemic injury. Usually unnoticed Maintenance Recovery:
ATN Maintenance Stage Urinating/Quality of urine Edema? GFR? Electrolytes (K and Na) pH Casts Duration	Oliguria. Low Urine Osm. Fluid overload (edema) Increased Cr/BUN, Increased K. High Na excretion. Anion Gap Met Acidosis (because of retention of H and anions). Muddy Brown Casts. Last 1-3 days
ATN Recovery Stage Urinating/Quality of urine Electrolytes	Diuresis, Hypotonic urine, Low K, Mg, PO4, and Ca
Renal Papillary Necrosis What is happening? Urine? Triggered by Associated with	Sloughing of renal papillae Gross hematuria and proteinuria May be triggered by a recent infection or immune stimulus Associated with DM, Acute Pyelonephritis, Chronic Phenacetin Use (acetaminophen) Sickle Cell Anemia
Acute Renal Failure (Acute Kidney Injury) \| Definition	Abrupt decline in renal function with ↑ Cr and ↑ BUN over several days
Prerenal azotemia Result of BUN/Cr ratio	↓RBF --> ↓GFR \| BUN/Cr ↑
Intrarenal azotemia Generally due to Less commonly due to Mechanism Casts BUN/Cr	Generally due to ATN or ischemia/toxins Less commonly due to acute glomerulonephritis Necrosis --> debris obstructing tubule --> fluid back flow --> ↓GFR Epithelial/granular casts BUN/Cr ↓
Post Renal azotemia What causes obstruction? Develops only when obstruction is?	Due to outflow obstruction (stones, BPH, neoplasia, congenital abnormalities) Develops only with bilateral obstruction
Prerenal Azotemia Urine Osm (mOsm/kg) Urine Na (mEq/L) FENa BUN/Cr	Urine Osm (mOsm/kg) > 500 Urine Na (mEq/L) < 20 FENa < 1% BUN/Cr > 20
Intrarenal Azotemia Urine Osm (mOsm/kg) Urine Na (mEq/L) FENa BUN/Cr	Urine Osm (mOsm/kg) < 350 Urine Na (mEq/L) > 40 FENa > 2% BUN/Cr < 15
Postrenal Azotemia Urine Osm (mOsm/kg) Urine Na (mEq/L) FENa BUN/Cr	Urine Osm (mOsm/kg) < 350 Urine Na (mEq/L) > 40 FENa > 2% BUN/Cr > 15
Consequences of Renal Failure Na/Water K pH Urea Blood Bones Lipids Growth	Na/Water retention --> CHF, Pul Edema, HTN) HyperK Met Acidosis Uremia Anemia (low EPO) Renal Osteodystrophy Dyslipidemia (↑ Tris) Growth retardation and developmental delay (children)
Uremia Blood work Presentation	↑BUN and ↑Cr \| Nausea, anorexia, Pericarditis, Asterixis, Encephalopathy, Platelet dysfunction
Renal Osteodystrophy \| Pathogenesis	Low VitD + Kidney dysfunction --> ↓Ca and ↑PO4 --> ↑PTH --> bone resorption (subperiosteal thinning of bone)
Adult PKD Gross presentation of kidney Presentation Genetics w/ chromosome Death from Associated with	Multiple, large, bilateral cysts Flank pain, hematuria, HTN, Urinary infections, Progressive renal failure Autosomal Dominant in PKD1 or 2 on chromosome 16 Death from chronic kidney disease or HTN (↑ Renin) Associated with Berry Aneurysm, MVP, Benign Hepatic cysts
AR PKD Genetics Associated with Significant renal failure in utero leads to Concerns beyond neonatal period	Autosomal recessive Associated with hepatic fibrosis In utero --> Potters Beyond neonatal concerns --> HTN, Portal HTN, Progressive renal insufficiency
Medullary Cystic Disease Genetics What does it lead to Inability to Visualization? On US Prognosis	Autosomal dominant Leads to tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine Medullary cysts usually not visualized US: shrunken kidney Poor prognosis
Renal Cell Carcinoma Originates from what kind of cells? Histo Most common in Risk ↑ w/ Presentation How does it spread Metastasizes to	Originates from PT cells Polygonal clear cells (accumulated lipids and Carbs) Most common in Men 50-70 Risk ↑ w/ smoking and obesity Hematuria, palpable mass, polycythemia, flank pain, fever, wt loss Renal vein --> IVC Lung and Bone
Renal Cell Carcinoma Frequency Genetics Tumors secrete? When is it usually detected? Treatment	Most common renal cancer Gene deletion in chromosome 3 (sporadic or von Hippel Lindau) Paraneoplastic (EPO, ACTH, PTH) Silent cancer because retroperitoneal. Usually detected b/c of metastases Resection. Resistant to Chemo and Radiation
Wilms' Tumor (Nephroblastoma) Frequency Contains what kind of structures Presentation Genetics Associated with what Syndrome?	Most common renal malignancy of early childhood (2-4) Contains embryonic glomerular structures Presents with huge palpable flank mass and/or hematuria Deletion of tumor suppressor WT1 on chromosome 11 May be part of Beckwith-Wiedemann Syndrome
Components of Beckwith-Wiedemann Syndrome	WARG \| Wilms, Aniridia, Genitourinary malformations, Retardation
Transitional Cell Carcinoma Frequency Can occur in Presentation Associated with...	Most common tumor of urinary tract system Can occur in Calyces, pelvis, ureters, bladder Painless hematuria (no casts) "problems in the Pee SAC" Phenacetin, Smoking, Aniline dyes, Cyclophosphamide
Acute Pyelonephritis Which part of kidney affected? Presentation Urine?	Affects cortex with sparing of glomeruli and vessels Fever, CVA tenderness, nausea, vomiting White cell casts in urine
Chronic Pyelonephritis Result of Requires Histo Tubules contain	Result of recurrent episodes of acute pyelonephritis Requires predisposition to infection (vesicoureteral reflux, chronic kidney stones) Coarse, asymmetric corticomedullary scarring and blunted calyx Tubules can contain eosinophilic casts (thyroidization of kidney)
Drug-Induced Interstitial Nephritis (tubulointerstital nephritis) Presentation Urine MoA Time course and drugs	Azotemia, fever, rash, hematuria, CVAT. Can be asymptomatic Pyuria (eosinophils) Drugs act as haptens --> hypersensitivity 1-2 weeks: Diuretics, penicillin, sulfonamide, rifampin Months: NSAIDs
Diffuse Cortical Necrosis What is it? Due to Associated with	Acute generalized cortical infarction of both kidneys Combination of vasospasms and DIC Associated with obstetric catastrophe (abruptio placentae) and Septic Shock
Which Nephrotic/Nephritic Syndromes have Subepithelial IC deposits	PSGN \| Membranous
Which Nephrotic/Nephritic Syndromes have Subendothelial IC deposits	MPGN I \| DPGN
Charges in the Tubule of the Kidney	Charges in the Tubule of the Kidney PT: -4 LoH: +7 DT: -10 CT: -50

USMLE - Renal Part 2

What ions does Aldosterone affect?

Key Terms

Related Flashcard Decks

Company

Explore

Study Tools