Renal & Repro Review Flashcards
Mesonephros becomes
WOlffian duct
epididymus
Metanephros becomes
uretric bud –> metanephric mesoderm –>
collecting duct
Major/minor calyxces
Renal pelvis
Metanephric blastema becomes
Glomeruli, bowman proximal tubule, loop of henle, distal convoluted tubules
Horseshoe kidney associated with what chromosomal syndromes
Turner syndrome
Trisomies 13, 18, 21
Rarely renal cancer
Unilateral renal agenesis due to
Absence of one kidney due to failure of ureteric bud to develop
No ureteric bud to induce differentaition ofmetanephric mesenchyme
Absence of kidney and ureter
Hydronephros
Dilated or thick walled bladder on ultrasound
Posterior urethra valves
Membrane remnant in the posterior urethra in males
Leads to urethra obstruction
What kidney is taken during donor transplantation?
Left kidney due to longer renal vein
Renal blood flow (10 steps)
- Renal artery
- Segmental artery
- Interlobar artery
- Arcuate artery
- Interlobular artery
- Afferent arteriole
- Glomerulus
- Efferent arteriole
- Vasa recta/ peritubular capillaries
- Venous outflow
Course of ureters
- under/over
Under uterine artery or vas deferens
Plasma volume can be measured by
Radiolabeling albumin
Percentages Total body water ICF ECF Plasma Interstitial fluid
60% total
40% ICF
20% ECF
Of ECF
25% Plasma
75% Interstitial fluid
% of body weight
Basement membrane of glomerular filtration barrier composed of
Type IV collagen chains
Heparan sulfate
Serum creatinine begins to rise when
GFR declines to < 60
Renal plasma flow can be estimated using
para-aminohippuric acid (PAH) clearance
Filtration Fraction
FF= GFR/RPF
Prostaglandins on filtration
Prostaglandins Dilate Afferent arteriole (PDA)
Increase GFR
Increase RPF
No change FF
Angiotension II on filtration
Angiotensen II constrict efferent arteriole (ACE)
Increase GFR
Decrease RPF
Increase FF
GFR vs RPF
GFR: amount filtered
RPF: amount filtered and secreted
Changes in glomerular dynamics (GFR, RPF, FF)
1) Afferent arterole constriction
2) Efferent arterole constriction
3) Increase plasma protein concentration
4) Constriction of ureter
5) Dehydration
6) ACE inhibitors
7) NSAIDS
8) Prostaglandins
9) Angiotensin II
1) Afferent arterole constriction
Decrease GFR
Decrease RPF
No change FF
2) Efferent arterole constriction
Increase GFR
Decrease RPF
Increase FF
3) Increase plasma protein concentration (Fluid stays in arterole) Decreased GFR No change RPF Decreased FF
4) Constriction of ureter
( High hydrostatic pressure inside bowman capsule –> favor blood staying in capillaries)
Decrease GFR
No change RPF
Decrease FF
5) Dehydration (Less filtered or secreted) Decrease GFR Large Decrease RPF Increase FF
6) ACE inhibitors
- Dilates efferent
Decrease GFR
Increase RPF
Decrease FF
7) NSAIDS
- Constrict Afferent
- Decrease GFR
- Decrease RPF
- No net change FF
8)Prostaglandins
- Dilate afferent
Increase GFR
Increase RPF
No change FF
9) Angiotensin II
- Constrict efferent
Increase GFR
Decrease RPF
Increase FF
Three stimuli for renin release
- beta-adrenergic stimulation (beta 1)
- Low Na in distal convoluted tubule
- Low pressure in afferent arteriole
Ureteric bud comes from
Caudal end of mesonephros (closest to feet)
Juxtaglomerular cells located
Inbetween afferent arteriole and distal tubule
Pregnancy effect on PCT
Decrease ability of PCT to reabsorb glucose and amino acids –> glucosuria and aminoaciduria
Concentration at which glucose spilled
Concentration at which tubular reabsorption of glucose saturated
Spilling at 160-200
Saturated at 350 mg/dL
First half proximal convoluted tubule primarily reabsorbs
Bicarb
Na
Relative concentrations along proximal tubule
Plasma Concentration Increases Unless Cleared by Kidneys
PAH Creatinine Inulin Urea Chloride Potassium
Sodium
HCO3
Amino acids
Glucose
Na reabsorbed with
1) Early PCT
2) Late PCT
1) Early PCT
- Na/H (Na in/ H out)
- Na/ X (glucose, AA, lactate) (all in)
2) Late PCT
- Na/Cl (all in)
(Driven by Na/K atpase)
3) Thick ascending limb
- Na/K/ 2Cl ( all in)
What class of drugs inhibits the Na/2Cl/K symporter in thick ascending limb
Loop diuretics
Causes Isotonic water excretion
Two cell types of collecting duct and last segment of distal tubule
Fxn of cells
1) Principal cells
- reabsorb water and Na
- Secrete K
2) Intercalated cells
- secrete H or HCO3
- Reabsorb K
Intercalated cells
- Alpha: Secrete H
- Beta: Secrete HCO3
Alpha ketoglutarate in which part of nephron
Proximal convoluted tubule
Absorbed in thick ascending limb
Na, Cl, K
Ca and Mg sneak in between cells
Nephron impermeable to water
Thick ascending limb
ADH works on what receptors
V2 vasopressin receptors on principal cells of collecting tubule
Tells cells to insert aquaporins into lumen surface of cells
H20 reabsorption
Drug that works by entering Na channel and blocks aquaporin
Lithium
Aldosterone effect on principal cell intercalated cells of collecting duct
Acts on mineralocorticoid receptor –> mRNA –> protein synthesis
Principal cells: reabsorption of Na and secretion of K
- Increase apical K conductance
- Increase Na/K pump
- Increase epithelial Na channel activity –> lumen negativity –> K secretion
Intercalated cells: Stimulates secretion of H (alpha cells)
- negative lumen –> Increase H ATPase activity –> increase H secretion –> Increase HCO3/Cl exchanger activity
PTH works on
Early PCT- inhibits Na/PO4 3- cotransport
–> PO4 3- (phosphate) excretion
Early DCT
- Increase Ca/Na exchange –> Ca reabsorption
AT II effect on nephron
Stimulates Na/ H exchange in early PCT
Acetazolamide
- MOA
- Uses
- Side effects
Carbonic anhydrase inhibitor
- Carbonic anhydrase converts HC02 –> CO2 + H20
- Cant reabsorb bicarb without
- Excreted in urine
Minor diuretic effect
Altitude sickness
(over come respiratory alkosis more quickly)
Urine Alkalinization
Glaucoma
(Bicarb production draws water into eye)
Idiopathic intracranial HTN (pseudotumor cerebri)
Adverse
- Metabolic acidosis
- Sulfa allergy
First line tx Idiopathic intracranial HTN
Acetazolamide
Mannitol
- MOA
- Use
- Adverse
- Dont use in (2)
Osmotic diuretic
- Causes osmolar load to stay in filtrate
- Prevent reabsorption of water
- Excretion of water
Increase serum osmolarity and Na
Shock
Drug overdose
Acute angle-closure glaucoma
Elevated ICP
Adverse
- Dehydration
Dont use
- Anuric renal failure
- CHF
Loop Diuretics
- Examples (4)
- MOA
- Use
- adverse
Bumetanide
Ethacrynic acid
Furosemide
Torsemide
Inhibit Na/K/Cl cotransporter
Loops Lose calicum
Use
- CHF
- Pulmonary edema
- Nephrotic syndrome
- Cirrhosis
Adverse - sulfa allergy (except ethacrynic acid) - Hypokalemia - Gout - Ototoxicity ** - Nephrotoxicity ** Muscle weakness **
Tx Altitude sickness
Acetazolamide
Thiazide diuretic
- Examples (3)
- MOA
- Feature
- Use
- Side effect
Chlorthalidone
Hydrochlorothiazide
Metolazone
Inhibit reabsorption of Na and Cl
- reducing diluting capacity of nephron
Retain Calcium
Helps with osteoporosis
HTN (first line)
Side effect
- Hypokalemia
- Hyponatremia
- Hyperglycemia
- Sulfa allergy
Potassium sparing diuretics
- examples
- MOA
- Use
- Adverse
Aldosterone antagonist
- Spironolactone
- Eplerenone
Block Na channels
- Amiloride
- Triamterene
CHF
Adverse
- Hyperkalemia
- Arrhythmias
- Gynecomastia (antagonist androgen receptor)
- menstrual irregularities
(Not eplerenone specific to mineralocorticoid receptor)
Diuretic
1) Increases urinary NaCl
2) Acidosis
3) Alkalosis
1) Increases urinary NaCl
- All except acetazolamide
2) Acidosis
- Acetazolamide
- K spring diuretics
3) Alkalosis
- Loop diuretics
- Thiazide diuretics
Shifts K into cells –> hypokalemia
Insulin
Beta- agonist
Alkalosis
Cell creation/ proliferation
PTH effect on Vit D synthesis
Faciliates 1alpha-hydroxylase addinig second hydroxyl group to make 1,25 (OH)2 Vit D
ANP on kidneys
Released by heart due to increased atrial volume and atrial pressure
Constricts efferent arterioles and dilates afferent arterioles
Increase GFR
Diuresis
Drug that causes SIADH
Cant Concentrate Serum Sodium
Carbamazepine
Cyclophosphamide
SSRI
Locked in syndrome
Correct hyponatremia too quickly
Causes lysis of myelin and pons
Diabetes insipidus
- Due to
- Central
- Nephrogenic
Too little ADH effect
Cant concentrate urine
Central
- Abnormal ADH production by hypothalamus
Nephrogenic
- Kidneys unresponsive to ADH
Nephrogenic diabetes inspidius can be cause by what drugs
Lithium
Demeclocycline (cousin of tetracycline)
First line tx Nephrogenic DI
Hydrochlorothiazide
- causes dehydration so PCT will concentrate more
(Indomethacin: decrease renal blood flow)
(Amiloride: lithium induced Nephrogenic DI)
- blocks Na channels Lithium enters through
Tx for Lithium induced Nephrogenic Di
Amiloride
- Blocks Na channels LIthium enters thorugh
Depression of reflexes
Hypermagnesemia
Tx Central DI
Desmopressin
Causes of acidosis with elevated anion gap
MUDPILES
Methanol Uremia Diabetic ketoacidosis Propylene glycol Iron tablet/ Isoniazide Lactic acidosis Ethylene glycol Salicylates
Patient with kidney stones presents with hypokalemia and metabolic acidosis. Anion gap is normal. Urine pH is 5.7. Defect?
Renal Tubular acidosis Type I
- Hypokalemia
- pH > 5.5
Impaired secretion of H by alpha intercalated cells in the collecting tubule
Hypoventilation causes
Respiratory acidosis
Anion gap=
[Na] - [Cl]- [HCO3]
10-12 normal
Normal anion gap acidosis
HARDASS
Hyperalimentation Addison disease Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion
Metabolic alkalosis caused by (3)
Excessive vomiting
Diuretics
Hyperaldosteronism
Type 1 Renal tubular acidosis
- due to
- pH
- electrolyte
- Increased risk for
- causes (3)
- Location
Alpha intercalated cells in collecting tubule unable to secrete H
Urine pH > 5.5
Hypokalemia
Risk for calcium phosphate kidney stones (due to increased pH and increased bone turnover)
Causes
- Amphotericin B toxicity
- analgesic nephropathy
- congenital anomalies (obstruction) of urinary tract
Distal
Type 2 Renal tubular acidosis
- due to
- pH
- electrolytes (2)
- Location
- Risk for
- Causes
Proximal tubule defect of HCO3 reabsorption
Urine pH < 5.5
Hypokalemia
Hypophosphatemia
PCT
Risk for hypophosphatemic rickets
Causes
- Fanconi syndrome
- Carbonic anhydrase inhibitors
Type 4 Renal tubular acidosis
- due to
- pH
- Electrolytes
- causes
Often due to hypoaldosteronism
If Low not putting potassium into urine
Urine pH < 5.5
Hyperkalemia
(prevents PCT from generating NH4)
Causes
- decrease aldosterone production (ACE inhibitor, ARB, NSAID, heparin, cyclosporine)
- Aldosterone resistance (K sparing diuretics, obstruction nephropathy, TMP/SMX)
Henoch-Schonlein Purpura renal problem
IgA nephropathy
Increased AA, glucose, bicarb, phosphate in urine.
- Due to
- May cause
- Causes
Fanconi syndrome
Generalized reabsorptive defect in PCT
May result in metabolic acidosis (proximal renal tubular acidosis)
Wilson dis GLycogen storage disease Ischemia MM Drugs (ifosfamide, cisplatin, tenofovir, expired tetracyclines)
Urine pH < 5.5
Hypokalemia
- type
- due to
- other lab
Type 2 Renal tubular acidosis
Hypophosphatemia
Proximal tubule defect of HCO3 reabsorption
Serum pH > 7.45
Hypokalemia
No medications
Increased Renin
Increased Aldosterone
Increased urine Ca
Bartter syndrome
- AR
Reabsorptive defect in thick ascending loop of Henle
- affects Na/K/2Cl cotransporter
Serum pH > 7.45
Hypokalemia
Hypomagnesemia
Hypocalcuria
Increased Renin
Increased aldosterone
Gitelman syndrome
AR
Reabsorptive defect of NaCl in DCT
Serum pH > 7.45
HTN
Hypokalemia
Decreased aldosterone
Decreased Renin
Tx
Liddle syndrome
AD
Gain of function mutation
Increase Na reabsorption in collecting tubules
Tx Amiloride
Urine pH < 5.5
Hyperkalemia
- type
- due to
- lab
Type 4 Renal tubular acidosis
Due to hypoaldosteronism
Low so not putting potassium into urine
Prevents PCT from generating NH4
Serum pH > 7.45 HTN Hypokalemia Decreased aldosterone Increased cortisol
- Acquired from
- Tx
Syndrome of Apparent Mineralocorticoid Excess (SAME)
Hereditary deficiency of 11beta-hydroxysteroid dehydrogenase
- cortisol not converted to cortisone
Can acquire from glycyrrhetinic acid (present in licorice)
Tx: Corticosteriods
Dopamine affect on nephron
- secreted by
- promotes
- affects what parts
- effect
Secreted by PCT cells promotes natriuresis
At lose doses, dilates interlobular arteries, afferent arterioles and efferent arterioles
–> Increase RBF, little to no change GFR
Higher doses= vasoconstrictor
Part of nephron with lowest pH
What happens at low pH
Distal tubule
Collecting duct
Uric acid precipitates at low pH
RBC cast
Glomerulonephritis
Malignant HTN
WBC cast
Tubulointerstitial inflammation
Acute pyelonephritis
Transplant rejection
Fatty casts
Nephrotic syndrome
Assoc w/ Maltese Cross sign
Granular (Muddy brown) casts
Acute tubular necrosis
Waxy casts
End-stage renal disease
Chronic renal failure
Hyaline cats
Nonspecific
Concentrated urine samples
Membranous means
Thickening of glomerular basement membrane
Nephritic (5) vs Nephrotic (5)
- due to
- features
Nephritic
- Due to GBM disruption
- HTN
- Increased BUN/Cr
- Hematuria
- RBC in urine
- proteinuria < 3.5
- Azotemia ( high nitrogen containing compounds, urea, creatinine)
- Oliguria ( low urine output)
Nephrotic - Podocyte disruption --> charge barrier impaired - Proteinuria > 3.5 g/ day - Hypoalbuminemia - Hyperlipidemia - Edema (Frothy urine with fatty casts)
URI 2 weeks ago Child Periorbital edema proteinuria <3.5 Cola-colored urine HTN
- Disease
- LM
- IF
- EM
- Type rxn
- decrease level
Acute poststreptococcal glomerulonephritis
LM
- gomeruli enlarged and hypercellular
IF
- “starry sky” granular appearance
- “Lumpy-bumpy” due to IgG, IgM and C3 deposition along GBM and mesangium
EM
- subepithelial immune complex (IC) humps
Type III hypersensitivity rxn
Decrease complement levels (C3) due to consumption
Nephritic syndrome seen in Good pasture syndrome
- clinical
- Seen on IF
- type hypersensitivity
Rapidly progressive (crescentic glomerulonephritis)
Hematuria
Hemoptysis
Type II hypersensitivity txn
Antibodies to GBM and alveolar basement membrane
–> Linear IF
Rapidly deteriorating renal function (days to weeks)
LM?
Consist of
Disease associated?
Rapidly progressive (crescentic) glomerulonephritis)
LM and IF- crescentmoon shape
Crescents consist of fibrin and plasma protein (C3b) with glomerular parietal cells, monocytes and macrophages
Nephritic syndrome seen with Granulomatosis with polyangiitis (wegener)
Rapidly progressive (crescentric) glomerulonephritis
Renal disease associated with SLE
Diffuse proliferative glomerulonephritis
Wire loop
Diffuse proliferative glomerulonephritis
- Due to
- LM
- EM
- IF
SLE
LM
- “wire looping” of capillaries
EM
- subendotthelial and sometimes intramembranous IgG based ICs often with C3 deposition
IF
- granular
Episodic gross hematuria that occurs concurrently with respiratory or GI tract infections.
LM
EM
IF
Assoc with
IgA nephropathy (Berger disease)
LM
- Mesangial proliferation
EM
- mesangial IC deposition
IF
- IgA based IC deposits in mesangium
Henoch Schonlein purpura
Retinopathy or lens dislocation
Glomerulonephritis
Deafness
- disease
- inheritence
- mutation
- MOD
- EM
Alport syndrome
X linked dominant
Mutation in type IV collagen
Thinning and splitting of glomerular basement membrnae
Basket weave appearance on EM
Membranoproliferative glomerulonephritis
- Type I (IF, appearance, Due to, assoc w/)
- Type II (also called, assoc with
Type I
- subendothelial immune complex (IC) deposits with granular IF
- Tram track appearance on PAS stain
- Due to GBM splitting caused by mesangial in growth
- May be secondary to Hep B or C infection
Type II
- Also called dense deposit disease
- Associated with C3 nephritic factor (IgG antibody that stabilizes C3 convertase –> persistent complement activation –> decrease C3 levels)
Nephrotic syndrome in children
Recent infection or immunization
- Disease
- LM
- IF
- EM
- Tx
Minimal change disease (lipoid nephrosis)
LM
- normal glomeruli (lipid may be seen in PCT cells)
IF
- negative
EM
- effacement of foot processes
Corticosteriods
Nephrotic syndrome associated with HIV, sickle cell
LM
IF
EM
Most common in
Focal segmetnal glomerulosclerosis
LM
- segmental sclerosis and hyalinosis
IF
- often negative but may be positive for nonspecific focal deposits of IgM, C3, C1
EM
- Effacement of foot process similar to minimal change disease
African americans and hispanics
Membranous nephopathy (membranous glomerulonephritis)
LM
IF
EM
Common in
Caused by
- primary
- secondary
LM
- diffuse capillary and GBM thickening
IF
- Granular as a result of immune complex deposition
EM
- Spike and dome with subepithelial deposits
Caucasian adults
Primary
- Ab to phospholipase A2 receptor (PLA2R)
Secondary
- NSAIDs
- Infectiosn (HBV, HCV, Syphilis)
- SLE
Poor responds to steroids
Diabetic glomerulonephropathy
LM
Pathogenesis
LM
- mesangial expansion
- GBM thickening
- Eosinophilic nodular glomerulosclerosis ( Kimmelstiel-Wilson lesions)
Nonenzymatic glycosylation of GBM –> increased permeability, thickening
Nonenzymatic glycosylation of efferent arterioles (hyaline arteriosclerosis) –> increase GFR –> mesangial expansion
Uric acid stones where
Xray findings
Crystal formation
Collecting duct
RadiolUcent
Rhomboid or rosettes
Cystine crystals
- xray findings
- shape
- test
Radiolucent
Hexagonal
Sodium cyanide nitroprusside test
Hydronephrosis due to
Distention or dilation of renal pelvis and calyces
Usually caused by urinary tract obstruction (e.g renal stones, sever BPH, cervical cancer)
Renal cell carcinoma
- originates from
- cell description
- color
- Clinical presentation
- Invades (may cause)
- Spreads to
- Tx
- Associated gene
- Assoc paraneoplastic
Originates from PCT cells
Polygonal clear cells filled with accumulated lipids and carbohydrates
Golden yellow due to high lipid content
Hematuria Palpable mass Secondary polycythemia Flank pain Fever WL
Invades renal vein
(May develop varicocele if left sided)
Spreads to IVC and spreads hematogenously –> lung and bone
Surgery
Immunotherapy (aldesleukin)
Gene deletion chromosome 3
(Sporadically or part of VHL disease)
Associated with paraneoplastic syndromes (ectopic EPO, ACTH, PTHrP, renin)
Polycythemia, Anemia, Hypercalcemia
Well circumscribed mass with central scar in kidney
- is what
- description
- seen with
Renal oncocytoma
- benign epithelial cell tumor arising from collecting ducts
Large eosinophilic cells with abundant mitochondria without perinuclear clearing
Arranged into nests
Large palpable unilateral flank mass on child
Hematuria
- contains
- mutation
Wilms tumor
(Nephroblastoma)
Contains embryonic glomerular structures
Loss of function mutation of tumor suppressor genes WT1 and WT2 on chr 11
Three syndromes that have wilms tumors
1) WAGR complex
- Wilms tumor
- Aniridia (absence of iris)
- Genitourinary malformation
- Mental retardation
(WT1 deletion)
2) Denys-Drash
- Wilms tumor
- Early onset nephrotic syndrome
- Male pseudohermaphroditism
(WT1 mutation)
3) Beckwith-Wiedemann
- Wilms tumor
- Macroglossia
- Organomegaly
- Hemihyperplasia (enlargement one side)
(Wt2 mutation)
Tumor of urinary tract system
- presentation
- seen in urine
Transition cell carcinoma
Painless hematuria
No casts
Squamous cell carcinoma of the bladder risk factor
Schistosoma haematobium infection (middle east)
Stress incontinence
Outlet incompetence
- Urethral hypermobility
- Intrinsic sphincteric deficiency
Leak with increase intra-abdominal pressure
Urgency incontinence
Tx
Overactive bladder
- detrusor instability
Leak with urge to void immediately
Tx: Antimuscarinics (oxybutynin)
Urinary incontinence associated with MS
Urgency incontinence
Overflow incontience
Tx
Incomplete emptying
- detrusor underactivity
- Outlet obstruction
Leak with overfilling
Increased post void residual
Tx
- Catheterization
- Relieve obstruction (alpha blocker BPH)
Seen in chronic pyelonephritis
Coarse, asymmetric corticomedullary scarring blunted calyx
Tubules can contain eosinophilic casts resembling thyroid tissue
Hypocalcemia Hyperphosphatemia Thinning of bones Bone lesions Hyperparathyroidism
Renal osteodystrophy
Failure of Vit D hydroxylation associated iwth chronic renal disease
- secondary hyperparathyroidism
> 20:1 BUN/CR
Prerenal
<15:1 BUN/CR
Intrinsic renal
Consequences of renal failure
MAD HUNGER
Metabolic acidosis Dyslipidemia (increased TGs) Hyperkalemia Uremia (Increased BUN) Na/ H20 retention (HF, pulm edema, HTN) Growth retardation Erythropoietin failure (anemia) Renal ostodystrophy
A patient is recovering at the hospital from a
suspected bacterial pneumonia. Over the
course of a few days he develops fever, rash, dysuria, and urinary urgency. Urinalysis shows a specific gravity of 1.001 with hematuria and mild proteinuria. Renal biopsy shows partial effacement of the tubulointerstitial structures
with pronounced edema and infiltration of the
interstitium with polymorphonuclear leukocytes, eosinophils, and lymphocytes with papillary necrosis. What is most likely to have
caused this condition?
(A) Antibiotics
(B) Chronic hypertension
(C) Lead ingestion
(D) Multiple myeloma
(E) Wegener’s granulomatosis
A. Antibiotics
Acute interstitial nephritis
P’s
- Pee (diuretics)
- Pain free (NSAIDS)
- Penicillins and cephalosporins
- Proton pump inhibitors
- RifamPin
Part of nephron injured in nephrotoxic acute tubular necrosis
PCT
A 64-year-old man with a medical history significant for hypertension, hypercholesterolemia, and coronary artery disease comes to the emergency department because of blood in his urine, nausea, and vomiting. Urinalysis reveals reddish-colored urine with no RBCs, but is positive for granular casts and protein. A basic metabolic panel shows highly elevated BUN and creatinine levels with a BUN:creatinine ratio of 10:1, as well as severe uremia. He is declared to be in acute renal failure and placed on dialysis. This patient has recently started a new drug
prescribed by his family physician. Which of
the following is the most likely cause of this
patient’s renal failure?
(A) A β-blocker
(B) An autoimmune reaction
(C) A statin drug
(D) Trauma
C. A statin drug
Statin can cause rhabomyolysis
A 48-year-old man is hospitalized for shock after massive blood loss in a motor vehicle accident. On the patient’s second day in the hospital, his blood urea nitrogen (BUN) and creatinine levels begin to rise and he develops pitting edema to his knees. A subsequent urinalysis shows numerous granular casts. Which of the following is the most appropriate treatment? (A) Angioplasty (B) Broad-spectrum antibiotics (C) Corticosteroids (D) Fluids and dialysis (E) Use of ultrasound to remove blockage
D. Fluids and dialysis
Acute tubular necrosis secondary to ischemia of the epithelial cells of teh PCT
Granular casts**
Common agents that cause nephrotoxic acute tubular necrosis
MARCEL
Myoglobinuria (Crush injury or statin) Aminoglycosides Radiocontrast agents Cisplatin Ethylene glycol Lead
Renal papillary necrosis
- seen in tubules
- clinical presentation (2)
- due to
- Associated with (4)
Sloughing of necrotic renal papillae
- gross hematuria and proteinuria
Recent infection or immune stimulus
SAAD papa with papillary necrosis:
- Sickle cell disease
- Acute pyelonephritis
- Analgesics (NSAIDS)
- Diabetes mellitus
ADPKD
- Presentation
- Mutation
- Death from
- Caused by
- Assoc with (4)
- Tx
Numerous cysts in cortex and medulla causing bilateral enlarged kidneys
PKD1 chr 16
PKD2 chr 4
Death from complications of chronic kidney disease or hypertension
- caused by increased renin production
Associated with
- Berry aneurysms
- Mitral valve prolapse
- Bengin hepatic cysts
- Diverticulosis
Tx
- ACE inhibitor
- ARBs
ARPKD
- Presentation
- Assoc with
- complications
Cystic dilation of collecting ducts
Infancy
Associated with congenital hepatic fibrosis
Potter sequence
Complications beyond infancy
- systemic HTN
- progressive renal insufficiency
- portal hypertension due to congenital hepatic fibrosis
ACE inhibitor
- Use
- Adverse
- Caution with
HTN
HF (decrease mortality)
Proteinuria
Diabetic nephropathy
In chronic kidney disease (diabetic nephropathy) decrease intraglomerular pressure –> slowing GBM thickening
Adverse (CATCHH)
- Cough
- Angioedema
- Teratogen
- Creatinine (increase, decrease GFR)
- Hyperkalemia
- Hypotension
Caution with patient that have bilateral renal artery stenosis, further decrease GFR
Aliskiren
- Type
- MOA
- Use
- Adverse
Direct renin inhibitor
Blocks conversion of Angtensinogen to angiotensin I
Use: HTN
Adverse
- Hyperkalemia
- Hypotension
- Angioedema
Brown urine
Subepithelial humps
Decrease C3
Post streptococcal glomerulonephritis
Red spots on butt and legs
Abdominal pain
Hematuria
Proteinuria <3.5
IgA Nephropathy
Which glomerular disease
1) Linear pattern of IgG deposition on IF
2) Lumpy-bumpy deposits of IgG, IgM, C3 in the mesangium
3) Deposits of IgA in teh mesangium
4) Anti-GBM antibodies, hematuria and hemoptysis
5) Crescent formation in the glomeruli
6) Wire loop appearance on LM
7) EM: Effacement of epithelial foot processes
8) Nephrotic syndrome assoc w/ Hep B
9) Nephrotic syndrome assoc with HIV
10 ) EM:Subendothelial humps and tram-track appeance
11) LM: Segmental sclerosis and hyalinosis
12) Purpura on back of arms and legs, abdominal pain, IgA nephropathy
13) Em: Spiking of the GBM due to electron-dense subepithelial deposits
1) Linear pattern of IgG deposition on IF
- Good pasture
2) Lumpy-bumpy deposits of IgG, IgM, C3 in the mesangium
- Post-streptococcal glomerulonephritis
3) Deposits of IgA in teh mesangium
- IgA nephropathy
4) Anti-GBM antibodies, hematuria and hemoptysis
- Good pasture
5) Crescent formation in the glomeruli
- Rapidly progressive glomerulonephritis
6) Wire loop appearance on LM
- Lupus nephritis
7) EM: Effacement of epithelial foot processes
- Minimal change disease
8) Nephrotic syndrome assoc w/ Hep B
- Membranous GN > Membranoproliferative
9) Nephrotic syndrome assoc with HIV
- Focal segmental glomerulosclerosis
10 ) EM:Subendothelial humps and tram-track appeance
- Membranoproliferative glomerulonephritis
11) LM: Segmental sclerosis and hyalinosis
- Focal segmental glomerulosclerosis
12) Purpura on back of arms and legs, abdominal pain, IgA nephropathy
- Henoch-Schonlein purpura
13) Em: Spiking of the GBM due to electron-dense subepithelial deposits
- Membranous nephropathy
Thickening of basement membrane
Spike and dome appearance
Membranous glomerulonephritis
SLE can cause
Train track
Subendotheial humps
Membranoproliferative glomerulonephritis
Glomerulonephritis assoc w/ Hep B and C
Membranoproliferative glomerulonephritis
Hematuria and proteinuria
Pulmonary infiltrates
Nasopharyngeal granulomas
c-ANCA
Granulomatosis with polyangiitis (wegener’s dis)
Urinary casts are made up of
Tamm-Horsfall mucoprotein
Secreted by tubule epithelial cells
Diffuse maculopapular rash
Azotemia
Eosinophilia
Fever
Acute interstitial nephritis (AIN)
Allergy induced
Drug induced
Urease producing bacteria
Proteus mirabilis
Klebsiella
S. saprophyticus
Struvite stones
Pee CHUNKSS Proteus mirabilis Cryptococcus H. pylori Ureaplasma Nocardia Klebsiella S. Epidermidis S. Saprophyticus
Renal tumor with clear cells
Renal cell carcinoma
Full of lipids/ carbs
Major risk factors transitional cell carcinoma
Smoking**
Aniline dyes
Naphthylamine dyes
Cyclophosphamide
Gene for thickened ectoderm at distal end of each developing limb bud
Wnt-7 gene
Gene for lengthening of limbs
FGF gene
Mutation in HOX presents as
Appendages in wrong locations