Usmle 1 Renal Physiology

• ▪ Renal System develops in the 1st trimester (12 weeks)
•    ▪ Fully functional b/c it produces amniotic fluid (20%)

▪ METANEPHROS - give rise to the kidney

▪ Differentiate from Mesonephros which evolves into the genitalia

▪ URETERIC BUD - gives rise to the entire collecting system

• ▪ Collecting duct, major and minor calices, papillae, hilum and ureters
• ▪ Otherwise can have renal agenesis

▪ Ureteric bud must make contact with the metanephros or kidney will NOT develop

• 

• • Cortex
•   • outermost layer
•   • Keeps isotonic urine
•   • same osmotic pressure

• • Medulla
•   • central layer of the kidney
•   • Keeps hypertonic urine
•   • higher osmotic pressure
•   • find packs of nephrons

• • Kidney Size
•   • 3 x 6 x 9 inches
•   • Left kidney is located at L1 (hilum)
•   • Right kidney is located at L2 (hilum)

• • In sickle cell anemia
•   • The patient has smaller vessels in the medulla → lose the ability to concentrate urine and therefore, one can infarct the kidneys sooner
• •
• 

• • Midwest → cooler climate = short nephron
•   • Dilutes urine → gets rid of H2O

• • California/any Hot area → Hot climate = SWEAT
•   • Longer nephron
•   • Need to hold on to water
•   • There is a high solute concentrated urine therefore, need to conserve water

• • The nephron will adjust and compensate in a week
•   • The nephrons elongate after 3-4 days
•   • That is why when you travel to a hot country you sweat a lot and then get adjusted as the time goes on

• • PCKD = polycystic kidney disease
• • Medullary sponge kidneys
• • Medullary cystic kidneys

• • Infantile
•   • AR
•   • Unilateral
•   • No Renal Failure
•   • No Hypertension

• • Adult
•   • AD
•   • Bilateral
•   • Renal Failure
•   • Hypertension

• Multiple cysts destroy the medulla

• • Polyuria (more pee than normal)
• • Polydipsia (great thirst)
• • Low volume state

• Occasional kidney stone

• Dx: Sonogram (bubbles)

• Many holes develop in the medulla

• • Polyuria (more pee than normal)
• • Polydipsia (great thirst)
• • Low volume state

• Multiple kidney stones

• Dx: Sonogram (holes)

• ­ ↑ incidence of Berry Aneurysms

• Posterior communicating artery in circle of Willis  is most commonly affected in these patients (recall that the MC is Anterior communicating artery)

• CN III is the most commonly affected

• subarachnoid hemorrhage(worse Headache of life)

• • renal conditions with which a child is born
•   • low volume state
•   • High pH will cause Ca to ppt → kidney stones.
•   • Polyuria, polydypsia, HTN
•   • Same electrolyte abnormalities

• • Medullary Cystic
•   • Sonogram will show bubbles
•   • many cysts destroy the medulla

• • Medullary Sponge
•   • Sonogram will show holes
•   • many holes develop in the medulla

• Alkalotic state causes Ca2+ to precipitate → Hypocalcemia and Stone formation

• One arm of the overlapping systems that regulate blood pressure and blood volume homeostasis

• • Step one: Angiotensinogen AT-I into circulation by the liver
•   • response to low blood pressure and adverse changes in sodium concentrations

• • Step two: Goes to Lungs
•   • AT-I converted to AT-II via ACE

• • Step three: AT-II stimulates
•   • alpha 1 vasoconstriction
•   • adrenals Z. Glomerlus)- Aldosterone release
•   • Posterior pituitary- ADH release
•   • CNS- thirst center

• • Step Four: Renin
•   • (JG cells-afferent) "Juxtaglomerular"

• JG cell hyperplasia with renin excess

• • No increase in blood pressure due to insensitivity
• of the presser effects of AT-II

• • Defect in the kidney's ability to reabsorb
• potassium

• • Excessive amount of potassium is excreted from
• the body. This is also known as potassium wasting

• • Metabolic acidosis, which causes a
• switch in H+/K+ pumps leading to K+
• leaving the cells and intering the serum.

• • Not a true hyperkalemia, just ions shifted in
• the wrong place.

• • Kidneys will recognize the high K+ and start
• to secrete it in the urine.

• (Hyperkalemia to Hypokalemia)

• • due to decreased gastrointestinal (GI) absorption
•    • (Diarrhea, malabsorption, diet)

• • increased renal loss
•    • diuresis due to alcohol, thiazides and loop diuretics

• • Think low flow→ renal artery stenosis
•   • Renin splits Angio I → Angio II
•   • ↓ Na due to dilution effect
•   • ↓ Cl
•   • ↓ K
•   • ↓ H+
• ­  • ↑ pH
•   • ↑ TPR → hypertension

• Think Low volume state

• • Common Causes
•   • Fibromuscular Dysplasia
•      • Under age 30
•   • Atherosclerosis
•      • Over age 40

• ↓ Blood flow because of ↑ resistance d/t vasoconstriction from the Renin system

• Therefore, velocity ↑ in order to get through occlusion, but the contralateral kidney is not protected = Goldblatt’s kidney

• • Goldblatt’s Kidney
•   • contralateral kidney is destroyed first when you have renal artery stenosis because renin will cause healthy kidney to be blasted with blood, while the affected kidney will have a clot protecting it.
•   • “Flea bitten kidney” → d/t burst capillaries
•   • Treatment:
•      • Remove contralateral kidney (nephrectomy)
•      • Remove ipsilateral blood clot (atherectomy)
•   • Most common cause of secondary hypertension

• Flow to the kidney is dependent on angiotesin II

• Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain Na and lose K and can constrict the glomerular mesangium, reducing the area for glomerular filtration

• • Severe stenosis → can’t give ACE inhibitor  because they will lose both kidneys
•   • ACE Inhbitors
•   • Ex. Patient on ACE Inhibitor will have ↑ creatinine indicating that the reason for hypertension is renal artery stenosis.
•   • Cox II inhibitors with sulfur
•      • Celecoxib
• • Loop diuretics
• • Sulfonoureas

• • All have sulfur- can cause allergy
•   • interstitial nephritis (spaces between the kidney tubules become swollen {cotex})
•   • hemolytic anemia
•   • G6PD

• ↓Angiotensin → ↓aldosterone → ↓Na reabsorption → ­↑Urine Na → ↓Serum Na → ↑depolarization

• • Also cause ­ ↑K → ↓depolarization
•   • Look for T wave

• • ACE also breaks bradykinin
•   • Causes cough
•   • Don’t need to stop unless it bothers patient.
•   • Benefit of bradykinin is vasodilatation
•   • Also causes proteinuria.

• C1 esterase inhibitor is affected in angioneurotic edema

#1Ca2+ 

#2 Struvite

#3 Uric acid

#4 Cystine stones

#5 Oxalate

• oxalate phosphate

• Hypercritical

• MCC: Normocalcemic hypercalciuria

• Treatment = thiazides

• Staghorn

• triple phosphate, Ca2+, Mg2+, NH4, Phos

• • MCC: Urease positive bacteria (UTI)
•   

"PUNCHS"

• • Proteus
• • Pseudomonas
• • Ureaplasma
• • Nocardia
• • Cryptococcus
• • H. pylori
• • Staph Saprophyticus

• Doesn’t show up on x-ray

• Severe flank pain (colicky pain) → pain comes in waves

• Most common cause = Dehydration b/c things start to crystallize

• • Any disease with high cellular death will predispose to uric acid stones
•    • burn pt, CA, massive trauma

• Chemotherapy can develop uric acid stones because of rapid cell turnover

Tx: normal saline, opiates for pain

• • Caused by 4 amino acids = COLA
•   • Cystiene
•   • Orinthine
•   • Lysine
•   • Arginine

• Envelope shaped crystals

• Look for family history

• • Prevention
•   • Hydration!!!

• • oxalosis
•   • Normal person will not have oxalate because:
•      • Usually comes from proteins break down in diet
•      • Ca will bind it and will defecate it out
•   • Malabsorption in GI tract will cause Ca2+ to get stuck in the fat and won’t be available to bind oxalate = saponification
•   • Ex. Oxalate stones in a 3 yo white male child indicates malabsorption due to CF. In blacks its celiac sprue.
•   • Ex. In a 32 yo female the most common cause of malabsorption is Crohns.  Look for diarrhea in history.

• IV normal saline

• • Opiates for pain
•   • < 5mm (½ cm)
•      • Let it pass
•   • 5mm to 1cm
•      • Lithotripsy (whorl pool)
•   • > 1cm
•      • Open laparotomy (i.e. struvate)

• Street- Heroin (short acting)

• For withdraws- Methadone (long acting)

• Kidney stones- Morphine

• • Abdominal pain- Meperadine
•    • no contraction of sphincter of odi

• • Percutaneous nephrostomy stent placement to drain the pus
•    • small, flexible rubber tube (catheter) through your skin into your kidney to drain your urine

• Dx: KUB; spiral CT; IVP

• Sonogram (if with hydronephrosis)

• Ureteroscopy- if stone is in the middle or lower 1/3 of ureter

• Glumeruli

• Tubules



• Interstitium

• Blood Vessels

• 20% of blood from the CO is going to the kidneys

• 90% of it, supply’s the cortex

• Only blood supply for the medulla - vasa recta

• Medulla- first place to infarct in a low volume state leading to medullary necrosis

• Answers:
• 

• More than one glomerulus are called glomeruli.

• 2 layers of cells = Vascular endothelium with it’s BM and then a Podocyte and it’s BM

• • Barriers in the glomerulus that prevent against proteinuria
•    • Negative charge of the BM
•        • heparin sulfate
•        • Albumin (negatively charged protein)
•    • The size of the fenestrations do not allow for large proteins to get through

• More than one glomerulus are called glomeruli.

• Consist of visceral epithelial cells (foot processes-podocytes)

• Glomular basement membrane (electron dense-type 4 collagen)

 

• Parietal epithelium lines bowman's space

• Fenestrae (in the endothelium)

• Most glomerular diseases are immunologically mediated.

• Proximal convoluted tubule (80% of reabsorption)

• Loop of Henely (triple transport)



• Distal convoluted tubule

• Collecting tubule (for concentrating the urine).

• Most tubular diseases are frequently caused by toxic or infectious agents

• In the cortex, comprising mostly of fenestrating capillaries (so any change in space, i.e. edema is abnormal).

• Most interstitial disorders are frequently caused by toxic or infectious agents.

• The filtrate absorbed in the glomerulus flows through the renal tubule, where nutrients and water are reabsorbed into capillaries.

• At the same time, waste ions and hydrogen ions pass from the capillaries into the renal tubule. This process is called secretion.

• The secreted ions combine with the remaining filtrate and become urine.

• The urine flows out of the nephron tubule into a collecting duct.

• It passes out of the kidney through the renal pelvis, into the ureter, and down to the bladder.

• Glomerular filtration rate (GFR)

• • Lab Filtration
•    • Filtration is measured by Inulin
•        • GFR = 1 / (Inulin)plasma

• • Physiological Filtration
•     • Filtration = 1 / creatinine

• • Lab Secretion
•    • Secretion = 1 / PAH

• • Physio. Secretion
•    • Secretion = 1 /BUN

• Measures RBF (renal blood flow)

• GFR =  = 20% of fluid that comes to the glomerulous.

• 20% of 1L (RBF) = 200 cc s

• Average Hct = 45 → subtract 45% of the blood from 200 cc → 125cc filtered/hour = GFR

• • 20 – 30 L of water comes through if left unrestricted
•    • But the nephron can reabsorb 95% of anything  that comes through.
•       • Therefore, 95% of 20 – 23 L = 3L of urine produced 

• Filtration Fraction (used for filtration of electrolytes)

   • FF =   (Renal plasma flow)

• Renal Failure

• • CL = FF – reabsorption + secretion
•    • Reabsorption – from the urine back to the plasma

• If CL < FF → Reabsorption > secretion

• • We rely on filtration to get rid of most drugs
•    • GFR dependent
•    • To decrease toxicity of most drug
•       • Need to ­GFR
•       • By ­ RBF, by giving IV fluids.
•    • Beware of giving nephrotoxic drugs to dehydrated patients.

• • Positive orthostatics
•    • 1 Have the patient lie down for 5 minutes. 
•    • 2 Measure blood pressure and pulse rate. 
•    • 3 Have the patient stand. 
•    • 4 Repeat blood pressure and pulse rate measurements after standing 1 and 3 minutes.

• • dry mucous membranes
• • increase for thirst
• • rapid heart rate
• • skin tenting (turgor, dehydrated)

• Determined by   (BUN: blood urea nitrogen)

• • Pre-renal Renal failure: → Low volume state
•    • Initial shock
•       • ↓ RBF → ↓ Clearance = NO GFR
•          • Serum Creatinine ↑
•          • Serum BUN ↑ because there is no secretion taking place
•          • ↑ BUN / ↑ Cr = Even ratio

   • Early phase of low flow to kidney will cause ratio to ­↑ overall

•    • Second phase will be: Angiotensin II constricts efferent more than afferent to create back pressure to ↑ GFR
•    • Cr ↓
•    • BUN ↑
•    • BUN / Cr Ratio > 20:1 = Pre-renal problem
•    • Urine Na < 10

• ↓ BUN

• ↑ Cr

• Initially ­↑ Cr but BUN will start falling.

• Then the vancomycin (or whatever is damaging the kidneys) will cause decrease filtration due to scaring and there will be no GFR or RPF so both serum Cr and BUN will rise. (no filtration or secretion occurring)

• Ratio is always less than 20:1

• • Post renal Failure
•   • “I haven’t pee’d in days!!!”
•   • No labs required
•   • MCC in adolescent = Urethral stricture
•   • Adult male = BPH
•   • Adult Female = Uterine prolapse

• • ↑ BUN:↓ Cr = Pre-renal failure
•     • 60/1.5 > 20:1
•     • LVS (dehy, burns, diarr)

• • ↑ BUN:↑ Cr = Renal Failure
•     • 60/3 = 20:1
•     • Drugs (gentamicin), Crystals (stones)

• • ↑ BUN:↑ Cr = Post renal
•     • 60/20 < 20:1
•     • Uterine prolapse, BPH

• • Tearing of RBC and platelets
•    • Petechiae (pinpoint, red round spots)
•    • Purpura (purple spots)
•    • Ecchymoses = large bruise

• • When a blood vessel tears
•    • CLOT FORMATION
•    • ↓ radius of the vessel             
•    • ↑ R = ↑ BP
•    • ↓ Flow to the kidney             
•    • Ischemia!!!!

• • Partial clot in renal artery
•    • renal stenosis

• • Complete clot in renal artery
•    • renal failure

• • Inflamed glomerulus
•    • glomerular nephritis

• • Clot off medulla
•    • interstitial nephritis

• • Clot off Papilla
•    • papillary necrosis

• • Clot of pieces of nephron
•    • focal segmental glomerular nephritis

• • Clot off all the nephrons
•    • RPGN = rapid progressive glomerular nephritis

• ▪ prevent proteinuria
•    ▪ neg charge of basement membrane
•       ▪ made of Heparin sulfate to repel albumin
•    ▪ Size of the pores is too small

• Hypertension

• • Macroscopic /Microscopic hematuria
•    • (smokey brown urine)

• • Oliguria (low urine output)
•    • foamy urine  

• • Edema 
•    • swelling caused by excess fluid trapped
•    • Ascites (fluid collects in abdomin)

• 24 hr urine collection

• • Leaky glomerulus lets proteins out
•    • Proteinuria >3.5g/day

• • GFR ↓ = auto immune
•    • check ANCA and anti-GBM

• Renal biopsy

Glomerulonephritis GN

• • Post Strep GN (streptococcus bacteria)
•    • MCC: Strep A

• Good Pasture GN (autoimmune disorder)

• • RPGN (Rapidly progressive glomerulonephritis)
•    • rapid loss of kidney function
•    • 50% decline in GFR

• • IgA Nephropathy (Berger's disease)
•     • IgA deposits build up causing inflammation

• Membranoproliferative GN (lesion during biopsy)

• • Membranous GN 
•    • small blood vessels in glomeruli, become damaged and thickened causing Prot leak

• • Minimal change disease
•    • large amounts of protein is lost in the urine
•    • 0-21 year olds

• Focal Segmental GN (scar tissue)

• Amyloidosis (amyloid build up)

• Mcc in children: minimal change disease

• Mcc in adults: membraneous nephropathy

• • Mcc in Blacks and Hispanics: FSGN
•    • Focal Segmental Glomerular Nephritis

• Fat cast

• • Hypertension, fluid overload and uremia
•    • Salt and water restrictions, diuretics and if
• needed dialysis

• • Inflammation of the glomerular
•    • corticosteroids

• • Diabetic
•    • ACE-I (↓ the progression of the disease)

• • Vaccinate (PPV 23)
•    • Strep pneumoniae infections

• Drug induced hypersensitivity
•    • Eosinophils
•    • (MCC: Cephalosporins)

• Globular nephritis
•    • RBC cast

• Infection
•    • WBC's
•    • Bacteria

• Uric Acid (Gout)
•    • Crystals

• Multiple myeloma
•    • Proteinuria (Bence jones)

• Myoglobinuria 
•    • Blood dipstick +, but no red blood cells

• Nephrotic syndrome
•    • Proteinuria > 3.5gm/d
•    • Fat cast

• 90% occur below the renal arteries

• MCC = Atherosclerosis

• Patient complains of a “ripping/tearing pain down the lower back”

• • Follow – up
•   • Sonagram/CT scan 
•   • if < 4 cm in size = follow every 6 – 12 months
•   • If  > 6 cm = control the HTN

• Occurs in the aortic arch

• MCC = Trauma >> Collagen Disease

• • Patient complains of upper back pain
•   • Type A → Ascending
•   • Type B → Descending

• Physical finding → Widened mediastinum on chest X-ray or Spiral CT

• Always control the HTN

• Clamp the aorta and pump the heart by hand = Open heart massage

• Do NOT do Chest compressions

• Pancreatitis → alcohol

• Kidney stones → painful heamturia

• AAA (abdominal aortic aneurysm) → Sever pain in lower back

• • Ischemic bowel
•   • There embolus (blood clot) to SMA (superior mesenteric artery)
•   • Bloody diarrhea d/t ischemia

• benign prostatic hyperplasia/hypertrophy

• Most common cause of urinary obstruction in adult men

• Obstruction is periurethral (central) : Dx DRE

• • Tx: terazosin or doxazosin (alpha 1 blockers) loosen sphinctor
•   • Tamsulosin (Flomax)- least side effects
•   • 2nd line - Fenesteride (block 5 alpha recductase)
•   • Sx –TURP (transurethral resection of prostate)

• dialation of the ureter due causes urine to reflux and back up

• • Unilateral
•   • Kidney stones

• • Bilateral
•   • Retroperitoneal fibrosis

• • Newborns → mal-implantation of the ureters
•   • Will cause oligohydramnios
•   • Treatment is surgery right away.

• • Children → UTI is the most common cause
•   • 3-4 weeks post-URI → reflux
•   • Rule:  1st UTI in male or 2nd UTI in female do a GU workup not kidney

• • Older women >40 → Most common causes
•   • uterine prolapse
•   • Cystocele

• • Older Man>40 → obstruction
•   • BPH → bilateral

• • Normally
•   • Detrusser muscle acts as a functional sphincter
•   • When it contracts urine cannot go back up the ureter

• • Composed of Smooth muscle
•    • Acts as a physiological sphincter

• • Histology
•    • TRANSITIONAL CELL EPITHELIUM

• • Able to hold 100 cc of urine before sending signals to urinate (Ca2+/Calmodulin – distention)
•   • If there is > 100 cc of urine in the bladder = obstruction
•   • When a patient complains of “frequency and urgency”
•     • = Bladder problem

• • Embryology
•   • Allantois → urachus → Bladder

• • Exstrophy of Bladder
•    • Fusion of lateral abdominal walls can catch the urachus and it gets stuck
•    • Therefore, a little piece of the urachus can extrude from the umbilicus 
•    • Urachus will protrude out of lateral abdominal fold = URACHAL CYST
•       • CLUE: urine drains from the umbilicus
•       • Predispose to bladder CA even after surgery
•       • Need surgery right away

• • At the tip of the bladder is the prostate
•   • Which explains why BPH patient complains of “frequency and urgency”
•   • Recall that the sphincters have α1 receptors

• • MC Bladder Mass = Diverticulum
•    • 2 Problems
•       • UTI
•       • Stone development
•       • Management:  Surgery

• • MC Bladder Tumor = Leiomyoma
•    • Mid line mass

• • MC CA = Transitional cell CA
•    • PAINLESS HEMATURIA
•    • Have multiple primary lesions
•    • Treatment: Cystectomy and radiation

The involuntary loss of urine

• Urge Incontinence

• Stress Incontinence

• Overflow Incontinence

• Detrusor muscle activity is increased.

• A spastic bladder ( UMN lesion)

• Bladder capacity is low due to repetitive bladder emptying

• Sphincter pressure is normal

• Gotta go…gotta go…gotta go

• • Tx:
•   • Imipramine (in children) TCA
•   • Oxybutynin (in adults) Blocks Ach (M)
•       (to decrease bladder contractions)

• • Tx: have patient urinate around the clock beginning with…
•   • hourly for 2 to 3 days,
•   • then every 2 hours for 2 to 3 days,
•   • then every 3 hours for 2 to 3 days,
•   • then every four hours (normal)

• MCC: obesity; estrogen connection

• Due to weak pelvic floor muscles

• Estrogen connection

• • Any increase in abdominal pressure
• ( like from sitting down, laughing, coughing,
• sneezing, etc) causes a sudden loss of urine

• Detrusor muscle function is normal

• Bladder capacity is normal

• Sphincter pressure is decreased

• • Tx: weight loss; Kegle exercises to tighten up pelvic floor muscles
•   • Use pseudoephedrine to tighten up the sphincter (alpha adrenergic)
•   • Suggest diapers or panty liners in the meantime

• Due to an anatomical obstruction

• • Detrusor muscle activity is decreased due to
• stretching

• Bladder capacity is increased

• Sphincter pressure is increased

• Sx: a weak urine stream; dribbling after urination; urgency; frequency

• Tx: surgically remove the obstruction

• In newborns: posterior urethral valves

• In children: strictures

• In adult men: BPH

• In adult women: uterine prolapse and cystoceles

• • Hypospadias
•   • Most common urogenital/congenital abnormality
•   • Normally the penis forms from dorsal → ventral (top → bottom)
•      • It closes from the tip to the base of the penis (penis fuses and zips all the way down)
•   • 90% of hypospadias occur in at the base of penis right next to the anus
•   • Most common complication:
•      • UTI (E. Coli, Proteus, Klabsiella)
•         • Enterococcus is the only nitrite negative UTI

• • Schistosomiasis
•   • (+) Squamous cell CA d/t chronic irritation

• • Posterior Urethral valves
•   • Most common cause of congenital bladder outlet obstruction in the newborn
•   • Every time bladder contracts, the valves close up
•     • These valves should be in the urethra to prevent reflux.

• Ballanitis

• Phimosis

• Paraphimosis

• Cystitis: ( urgency and frequency)

• Pyelonephritis 

• • Nephritis (inflammation of nephron)
•   

• • Ballanitis
•   • Infection of the head of the penis. (Staph aureus)
•     • Rx:  Clindymycin
•     • Macrolides
•     • Amoxicillin and clauvanic acid

• • Phimosis
•   • Infection and scarring of the foreskin at the head of the penis (tip)

• • Paraphimosis
•   • Infection and scarring of the foreskin at the bottom of the penis (base)
•     • Most common cause of circumcision:
•       • Cosmetic
•       • Decreased risk of UTI, and penile CA
•       • Best time to circumsize is 48 hours after birth because nerves haven’t developed yet

• • Pyelonephritis →infection goes up through the kidney and into bloodstream
•   • Sepsis
•   • WBC casts
•   • Ascending infection

• • Nephritis (inflammation of nephron)
•   • Pyelonephritis = WBC casts and sepsis
•   • Glomerulonephritis = vasculitis → hematuria & RBC casts
•   • Interstitial nephritis = allergy to kidney (think about drugs)

• Infection of the urethra

• Dysuria by itself as a symptom

• Most common cause is Chlamydia (90% asymptomatic, Gonnorhea is symptomatic)

• • Rx: 
•   • 1 dose treatment for Gonorrhea
•      • Ciprofloxacin – 500 PO
•      • Ofloxacin – 400 PO
•      • Gatafloxacin – 400 PO
•      • Ceftriaxone – 250 IM - DOC
•      • Cefixime – 400 PO
•      • Cefoxitine – 250 IM
•   • 1 dose treatment for Chlamydia = Azithromycin
•      • 1gm or 2gm

If you have Gonorrhea must cover for Chlamydia

• E.coli

• Proteus → Urease (+), Struvite stones, high urine pH, swarming motility

• Klebsiella

• WBC casts: nephritis

• RBC casts: glomerulonephritis

• Eosinophil casts: interstitial nephritis

• Fat casts: nephrotic syndrome

• Waxy casts: chronic renal failure

• Hyaline and epithelial casts: normal findings;represent sloughed off cells, most from the PCT

• Crescents: RPGN. Goodpasture’s or Wegener’s

• Pyelonephritis: Sepsis

• ▪ Type I: distal H/K exchange is defective
•   ▪ Urine pH is very high; renal stones; UTIs

• ▪ Type II: proximal CA does not work
•   ▪ Urine pH is very high ( distal H/K exchange still works)
•   ▪ Can not reabsorb HCO3-

• ▪ TYPE III: combines the above two
•   ▪ Urine pH is normal

• ▪ Type IV: hyporenin-hypoaldosterone syndrome
•   ▪ Seen in diabetics; JG apparatus is infarcted

▪ pH vs HCO₃^-

▪ If the patient’s pH is acidic, you should expect that patient’s HCO3- to be low(buffering)

• ▪ If not, then the problem has to be: respiratory

• ▪ Hyperkalemia
• ▪ Respiratory PaCO₂ ↑   (Pa = Partial pressure)
•   ▪ HCO₃^- ↑ (compensations)
•   ▪ HCO₃^- normal (non-compensation)

• ▪ Metabolic HCO₃^- ↓
•    ▪ PaCO₂ ↓ (compensation)
•    ▪ PaCO₂ normal (non-compensation)

▪ Hypokalemia

• ▪ Respiratory PaCO₂ ↓   (Pa = Partial pressure)
•    ▪ HCO₃^- ↓ (compensating)
•    ▪ HCO₃^- normal (non-compensation)

• ▪ Metabolic HCO3- ↑
•     ▪ PaCO₂ ↑ (compensating)
•     ▪ PaCO₂ normal (non-compensation)

• ▪ Arterial  pH 7.3 (ACID)
•                pCO2 30 mm Hg  ⇚
•                pO2 95 mm Hg

▪ Serum HCO3- 14 mEq/L (low)

▪ Metabolic Acidosis w/respiratory compensation

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