uterine artery

ductus deferens

"water under the brdige"

mesonephros

Also serves as the interim kidney during the 1st trimester

Describe the pathology of potter's syndrome:

Bilateral renal agenesis due to malformation of the ureteric bud leading to oligohydramnios

1. facial abnormalities: flattend nose, low-set ears, and recessed chin
2. pulmonary hypoplasia: amniotic fluid contributes the the development of the fetal lungs. infants with prolonged oligohydramios often suffere from respiratory distress due to pulmonary hypoplasia

1. Seminal vesicle
2. Epididymis
3. Ejaculatory Duct
4. Ductus Deferens

What is used to approximate the GFR?

why does this slightly overestimate GFR?

creatinine clearance is an approximate measure of GFR

it slightly overestimates GFR because creatinine is moderatly secreted by the renal tubules

what is responsible for dilating the afferent arteriole?

what effect does this have on GFR, RPF, and FF?

prostaglandins dilate afferent arterioles

RPF and GFR increase proportionally, so FF remains the same

how do you calculate renal plasma flow?

How do you calculate renal blood flow?

Renal plasma flow (RPF) = U_PAH x V/ P_PAH

                                     = clearance (PAH)

RBF = RPF / (1-hematocrit)

This part of the nephron actively reabsorbs Na+, K+ and Cl- and indirectly induces paracellular reabsorption of Mg2+ and Ca2+

Thick ascending loop of henle

how does PTH increase serum Ca2+ levels

1. increase Na/Ca²⁺ exchanger
2. induces 1alpha hydroxylase

1. Acute lung disease
2. Airway obstruction
3. Chronic lung disease
4. Opioids, narcotics, sedatives
5. Weakening of respitratory muscles

Conditions causing anion gap metabolic acidosis:

MUDPILES

Methanol

Uremia

Diabetic ketoacidosis

Paraldahyde Paraformin

Iron tablets or Isoniazid

Lactic acidosis

Ethylene glycol (oxalic acid)

Salicylates

Diahhrea

glue sniffing

renal tubular acidosis- addison's disease

hyperchloremia

Post Streptococal Glomerulonephritis

LM: lumpy-bumpy appearance, hypercellular, neutrophils

IF: IgG and C3

EM: subepithelial immune complexes

• Most frequently seen in children and present with peripheral and periorbital edema
• Most often following impetigo, or upper respiratory infection with group A strep (pyogenes)

Rapidly Progressive Glomerulonephritis (Crescentic)

LM: hypercellular and cresecent shape

IF: IgG/C3 arranged in a cresecent

This rapdily progresses to renal failure in weeks.

can be caused by goodpastures, wegeer's granulomatosis (c-ANCA), or microscopic polyarteritis (p-ANCA)

DX: Subendothelial immune complexes showing "wire looping" of capillaries

[image]

Diffuse proliferative glomerulonephritis (due to SLE)

IF: granular, subendothelial DNA/anti-DNA immune complexes

"Wire Looping" of capillaries: looks very similar to Post-strep GN except granular immune complexes are everywhere

Most common cause of death in SLE

[image]diffuse proliferative glomerulonephritis (SLE type IV)

notice the hypercellularity all over the glomerulus, and the wire-looping pattern.

Berger's disease (IgA nephritis)

This is a variant of Henoch Schonlein: palpable purpura in bottocks, back of legs, polyarthritis, GI bleed and hematuria (RBC casts)

Also associated with celiac sprue (due to increase secretion of IgA)

Dx: tram-track  splitting of BM on silver stain as well as hypercellularity, and mesangial cell proliferation

membranoproliiferative GN

Hypercellularity

proliferative= mesangial cell proliferation

membran= "tram-track" splitting of BM on silver stain

IF: C3

Type I: subendothelial deposit that produces nephrotic syndrome

Type II: auto-antibody agains c3 = C3 nephritic factor

causes converstase to become overactive and is constantly breaking complement down.

Dx: Spike and Dome appearance on silver stain

membrane-like capillary wall thickening

Diffuse membranous glomerulonephritis (membranous glomerulonephritis)

SLE's nephrotic presentation

Most common nephrotic disease in adults

LM: membrane-like capillary wall thikening, spikes on silver stain

IF: IgG/C3, granular and linear

EM: subepithelial deposits

Focal Segmental GS:

• Black people
• AIDS
• Sickle cell
• IVDA

Poor reponse to steroids, and often recurs in transplanted kidney

Nodular sclerosis/ Diabetic glomerulonephropathy

Non-enzymatic glycosylation of efferent arterioles increases GFR--> mesangial damage (hyperfiltration damage)

Wire-looping on Kimmelstiel-Wilson

Give ACE inhibitor to stop progression

Which nephrotic/nephritis syndrome is associated with?

• tram-track appearance due to GBM splitting caused by mesangial ingrowth
• Hepatitis B/C

membranoproliferative glomerulonephritis

can present as nephritic or nephrotic syndrome

Kidney stone that may result from ethylene glycol (antifreeze, metabolic anion gap acidois) or vitamin C abuse?

Ammonium magnesum phosphate (struvite)

• urease producing bugs increase pH. Condition is worsened by alkaluria
• may be radiopaque or radiolucent
• urease producing bugs can form staghorn calculi that can be a nidus for UTIs

uric acid renal stone

strong association with hyperuricemia (gout)

these form in low pH- Alkalainize urine with acetozolamide to stop them from forming

Cystine stones:

Cysteine, ornithine, lyseine and arginine all share the same transporters in the jejunum and in the proximal tubule. If thse transporters are not functiong, there will be a higher concentration of these AAs in the urine. Cysteine is the one that precipitates in low pH. Alkalinize urine with acetozolamide to treat

Prolactin

PTHrP

ACTH

EPO

WAGR:

Wilm's tumor

Aniridia- absent iris

Genitourinary malformations, Mental-Motor Retardation

Flank Mass

Hypertension due to renin production

pyelonephritis

• Asymmetric, corticomedullary scarring
• Blunted calyx
• tubules contain eosinophilic casts
• Flank pane and fever

• Acute generalized infarction of cortices of both kidneys
• likely due to a combination of vasospasm and DIC
• Associated with abruptio placentae and septic shock

Drug-induced interstitial nephritis

• penicilin derivatives, NSAIDs (phenacetin), diuretics: all act as haptens producing hypersensitivity
• hematuria
• acute interstitial renal inflammation leading to oliguria and eiosinophilia

Dx: granular, muddy-brown casts due to necrosis and epithelial cell detachment

what are a few causes of this?

Acute tubular necrosis

associated with renal ischemia, crush injury (myoglobinuria), toxins

diabetes mellitus

acute pyelonephritis

chronic phenacetin use

sickle cell anemia

• common, benign congenital disorder
• characterized by cystic dilations of the medullary collecting ducts (cysts don't involve renal cortex)
• usually asymptomatic

Fanconi's syndrome:

What are some causes?

decreased proximal tubule transport of amino acids, glucose, phophate, uric acid, proein and electrolytes.

can be caused by wilson's disease, glycogen storage diseases and drugs (cisplatin, expired tetracycline)

Decreased phosphate reabsorption

decreased HCO3- reabsorption

decreased Na+ reabsoption

Shigella and EHEC 0157:H7

1. acute renal failure (oliguria/anuria) microangiopathic
2. hemolytic anemia (pallor and red urine)
3. thromboytopenia