USMLE - Renal Part 1

Captopril, Enalapril, Lisinopril
CHF, HTN, Diabetes, Renal Disease
Cough, Angioedema, Teratogen, Cr Increase, Hypotension, HyperK
Do not use in Renal Artery Stenosis

Do not cause cough or angioedema because they do not affect inhibit Bradykinin degradation

Increased. Serum NaCl may decrease

All diuretics increase urine K except for KSD. Serum K may decrease

CAI (decreased bicarb reabsorption) and KSD (hyperK –> H leaving cells)

Loop and Thiazide
Decreased Vol –> ATII –> Na/H exchanger –> bicarb reabsorption (contraction alkalosis)
Decreased K –> H entering cells
Decreased K –> H (instead of K) exchanged for Na in CT

Spironolactone, Eplerenone, Amiloride, Triamterene
Increased Ald, Decreased K, CHF
S –/ Ald R, T and A –/ Na Channels
Increased K –> Arrhythmias, S –> gynecomastia + anti androgen

Urine Ca increases with LD and decreases with Thiazide

–/ NaCl reabsorption in DT
HTN, CHF, Increased Ca in Urine, Nephrogenic Diabetes Insipidus
Hyper Glucose, Lipids, Uric Acid, Ca
(HICC the GLUC)

Like Furosemade for people allergic to Sulfur

Furosemide
–/ NaK2Cl pump, –> PGE –> AA dilation
Inhibited by NSAIDs
Edema (CHF, cirrhosis, Nephrotic Syndrome, Pul Edema), HTN, Hypercalcemia
Ototoxic, HypoK, Mg and Ca, Dehydration, Alergy, Alkalosis, Interstitial Nephritis, Gout

Acetazolamide

Glaucoma, Make Urine Basic, Alkalosis, Altitude Sickness, Pseudotumor Cerebri

Met Acidosis (with increased Cl), Paresthesia, NH3 toxicity, Sulfa allergy

Shock, OD, ICP, IOP
Osmotic Diuretic
Pul Edema, Dehydration
Contraindicated in CHF, anuria

PT: reabsorbed, Descending LoH: secreted, CD: Reabsorbed or stays in lumen depending on ADH

ADH –> UT1 in medullary collecting to increase Urea reabsorption which adds to corticopappillary osmotic gradient

PT PTH –> 1 alpha hydroxylase (which converts 25 vit D to 1, 25 vit D)

Vit D –> Osteoblasts –> alkaline phasphatase
AP hydrolyzes Pyrophasphate and other inhibitors of Ca-PO4 crystallization.

GI reabsorption of Ca and PO4
Bone mineralization
Maintains serum [Ca]
–> monocytes to become osteoclasts

Anticoagulants (warfarin and heparin)
Cyclophasphamide –> hemorrhagic cystitis and increased risk for transitional cell carcinoma

Dipstick for albumin
SSA (sulfosalicylic acid) for albumin and globins

Increased GFR –> Decreased Urea reabsorption

Not associated with rena disease
fever, exercise, CHF, Orthostatic

LMW proteinuria

Multiple Myeloma, Hemoglobinuria, Myoglobinuria

Defect in PT reabsorbing LMW proteins

Hg or Pb poisoning

Fanconi Syndrome

Hartnup Disease

Prerenal azotemia

| Early postrenal azotemia

Causes Potter Syndrome
Extremity deformities, Facial deformities, Pulmonary hypoplasia
Incompatible with life

JG apparatus releases Renin and undergoes hypertrophy and hyperplasia (in order to secrete more renin)

JG cells = modified smooth muscle cells of AA and EA
Macula Densa = tall, narrow cells in DT
The MD responds to [Cl] (via NaK2Cl pump) and transmits this information to JG cells which respond by secreting Renin

2/3 reabsorbed in PT
20% in LoH
Secreted in CD unless in a low K state --> Intercalated cells reabsorb K (K/H exchanger)

High K diet, Aldosterone, Alkalosis (K/H exchanger), Diuretics (except KSD)

Benign tumor made of blood vessels, SM, and fat
Diagnosed with abdominal CT because of low density of fat
Associated with Tuberous Sclerosis

Type III: Immune Complex Mediated
After GAS infection, IC formed against bacterial antigens cross react w/ GMB and deposit in subepithelial portion of the glomerulus.
Lumpy Bumpy on IF and electron dense humps on EM

IMA

Increased Luminal Flow
ATII (decreased cAMP)
NE (via PKC)

DA

| PTH (increased cAMP)

Week 4

1st Trimester

Week 5

| Nephrogenesis continues through week 32-36

Male: Mesonephros --> Wolffian duct --> ductus deferens and epididymis
Female: --> Gartners ducts

Collecting Duct, Calyces, Pelivs, Ureter

| Fully canalized by week 10

Glomerulus through collecting tubule

Ureteropelvic junction

Ureteropelvic Junction

ARPKD, Posterior Urethral Valves, Bilateral Renal Agenesis

Turners Syndrome

Due to abnormal interaction bet ureteric bud and metanephric mesenchyme
Leads to non functional kidney
Kidney consists of cysts and connective tissue
Unilateral
Asymptomatic
Diagnosed by prenatal US

Left because of longer renal vein

Ureter goes Under uterine artery and ductus deferens

| water under the bridge

60% water --> 2/3 intracellular, 1/3 extracellular

| 1/4 plasma, 3/4 interstitial

radiolabeled albumin

Inulin

290 mOs/L

Fenestrated capillaries (size)

Fused BM with heparin sulfate (neg charge barrier)

Podocyte foot processes (epithelium)

Lost

C = UV/P

Reabsorption

Secretion

Slight overestimation because Cr is secreted

100ml/min

C inulin, C creatinine, or K[(Pgc-Pbs)-(Pigc-Pibs)]

PAH because it is filtered and actively secreted. All PAH that goes in goes out

C pah

RPF/(1-Hct)

ERPF underestimates RPF by ~10%

GFR/RPF

GFR x Px

NSAIDs --/ Prostaglandins (which normally dilate AA)

| NSAIDs --> Decreased RPF and GFR --> no change in FF

ACEI --/ ATII (which normally constricts EA)

| ACEI --> Increased RPF, Decreased GFR --> Decreased FF

RPF: Decreases
GFR: Decreases
FF: NC

RPF: Decreases
GFR: Increases
FF: Increases

RPF: NC
GFR: Decreases
FF: Decreases

RPF: NC
GFR: Increases
FF: Increases

RPF: NC
GFR: Decreases
FF: Decreases

V x U

Filtered - excreted

Excreted - Filtered

160mg/dL

350mg/dL

Can reduce reabsorption of Glucose and AA

Deficiency of neutral AA (Tryptophan) transporter in PT

| Leads to Pellagra

NH3 as a buffer for secreted H+

Inhibits Na/PO4 cotransporter --> PO4 excretion. Will also decrease Na reabsorption in PT
--> cAMP and IP3

ATII --> Na/H exchanger --> increased Na, H2O and Bicarb reabsorption
ATIIR --/ cAMP, ATiiR --> IP3
Can lead to contraction alkalosis

PTH --> Na/Ca exchanger in basal membrane --> Increased Ca Reabsorption

V2 receptor on Principal Cells

Increases in Concentration by not Amount because of water reabsorption

Occurs at a slower rate than Na reabsorption in the proximal 1/3 and then matches Na distally --> [Cl] increases then plateaus
Reabsorbed by Cl/Base exchanger

Decrease in BP, Decreased Na(Cl) delivery to DT, Increased Sympathetic tone (β1 Receptors)

Converts AT1 to AT2

| Degrades Bradykinin

• -> AT1 receptor --> Vascular SM constriction

• -> EF constriction

• -> Adrenal Cortex --> Aldosterone

• -> Post Pituitary --> ADH

• -> PT --> Na/H exchanger

• -> DT --> Na/Cl cotransporter

• -> Hypothalamus --> Thirst

ATII affects baroreceptors function to limit reflex bradycardia which would normally accompany its pressor effects

Released by atria in response to increased volume
ANP --> cGMP --> vascular smooth muscle relaxation --> increased GFR --> decreased renin release
Increased GFR --> Increased Na filtration (w/o compensatory Na reabsorption distally)
Net effect is Na and volume loss

ADH primarily regulates: Osm
Will also respond to: Vol
Which one takes precedence --> vol

Volume

BB --/ Beta1R in JGA

| Thereby BB --/ Renin release

EPO released by interstitial cells in the peritubular capillary bed in response to hypoxia

Paracrine secretion vasodilates the AA to Increase GFR

Released in response to Decreased Ca, Increased PO4, or Decreased VitD
Leads to Increased Ca reabsorption (DT), Decreased PO4 reabsorption (PT), and Increased VitD production

Decreased Vol (ATII)

Increased K