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Renal UrinaryMidterm

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					                                RENAL/URINARY MIDTERM REVIEW


This review is as per course objectives, as listed in course syllabus or listed on instructors‟ handouts.

GENERAL
Structure-Function, Symptoms (2,3)

Structure-Function (pp 31-9, pp 244-5)
Vascular
- End arteries: segmental infarcts, RHTN, stenosis…
- Receive ¼ of cardiac output => a drop in BP or diversion of blood for activity or digestion reduces
           urinary output.
- 2 million nephrons at birth, lost during disease => renal function blood tests do not change until only ½
           million remain
- Filtration system is so enormous that GU infex may happen days/weeks after original => a history of
           cold, cough, sore throat, dental work, skin abscess… will indicate which a’biotic to use,
           before cultures
- Renal arterioles do not anastamose => small ischemic segments sets off R-A mechanism --> raises BP,
           higher than necessary pressures in other kidney and systemically, hence treating HTN may
           compromise renal function
- Renal transplant can survive without neural connex => metabolic and hemodynamic effects influence
           the kidney
- Renal pedicle lymph nodes are first stop for metastasis from testicular cancer => due to embryological
           origin of blood and lymphatic supply of testes
- Caudally, the only support to the kidney is a pad of fat and loose connective tissue => they are
           suspended by great vessel attachments, so falls may result in unexpected vascular injury to
           kidneys

Parenchyma
- Nephron: cystic disease, glomerular and tubulo-interstitial diseases…
- Renal cystic disorders => genetic predisposition to cystic disease can affect renal function, BP,
         susceptibility to infex.
- Osmotic gradient => deep in medulla where chemicals are in nephrotoxic concentrations, such as
         glucose in diabetics, causing papillary necrosis

Medulla & Collecting Junction
- Forniceal sinus: ascending pyelonephritis…
- Fascia cribosa into minor calyx is not protected by sphincter; so increased calyceal pressure is transmitted
         to nephron => ascending pyelonephritis and renal lithiasis (Randall’s plaques)
- Renal protective measures:
     o Upward reflux of urine prevented by infundibular sphincter
     o Corollary sinus circumferentially surrounds the renal papilla, for reserve of excess urine =>
         kidney is protected days to weeks (21 days) in ureteral obstruction due to: calculus, ligation,
         trauma, prolonged delivery…

Pelvis-Ureteral System
- Ureteropelvic junction (UPJ): obstruction…
- Ureteral segments: calculi, viscero-viscero/viscero-somatic reflexes…
- Increased pressure from bladder up three ureteral segments will cause dilation of these segments =>
          X-ray appearance is called Cystoids, which protects the low-pressure upper tract from this
          devastatingly high lower tract pressure
- If protective measures fail and entire ureter becomes dilated and tortuous => the ureters bend, and these
          have been incorrectly called obstructive kinks




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Bladder
- Infection, continence/incontinence
- Ureters wind under vas deferens and obliquely into detrusor muscle, sensory nerve supply being shared by
          both => stone in distal ureter may cause pain in ipsilateral testicle, medial thigh, or perineum
- Bladder has defense mechanisms preventing ascending UTI‟s => a normally functioning bladder
          cannot be infected by installation of bacteria
- Bladder wall and fundus rich in -adrenergic receptors, whereas neck of bladder and proximal urethra are
          rich in -adrenergic receptors => bladder neck obstruction can be treated with -blockers;
          incontinence can be treated by reducing detrusor tone

Pelvic Floor
- Function of pelvic organs depends on structural balance of supporting structures => while treating target
         organ pathology be certain surrounding anatomy and function is normal (balance osseous
         structures, test/correct for muscle and fascial strains and tensions)

Urethra
- Female urothelium thins from decreased local estrogen levels in aging => easily treated
- Para-urethral glands secrete protective mucous to protect from bacteria in introit ascending into bladder
         => infex of these glands are source of post-coital infex, “Honeymoon cystitis,” pelvic floor
         syndrome, dyspareunia
- Male urethra => consider mechanics and symptom referral pattern from the urethra before
         considering the special conditions involving prostate


Reflexes (pp 31-9, Scientific Basis of Osteopathic Med.)
- Accommodation reflex = bladder relaxes, as filled, without increasing pressure
- Viscero-viscero, viscero-somatic

Terms/H&P
S/S
- Urgency, frequency, burning, dysuria (painful urination), tenesmus (bearing down to get last bit out)
- Nocturia (voiding at night) vs. nycturia (if volume voided at night is greater than during day)
     o Nocturia = sign of prostatic disease, obstructive disease, or infex
     o Nycturia = sign of renal disease/nephrosclerosis
- Incontinence:
     o Stress = sneeze, cough, laugh
     o Urge = leak a little before you get to the toilet
     o Dribbling = post-pee leftovers
     o Overflow = too much volume spills over
- Urosepsis, pyuria, bacteriuria, crystalluria, cylinduria (casts), pneumaturia, hematuria,
- Urethral discharge
     o Specific - gonorrhea
     o Nonspecific – chlamydia




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Approaching the Patient (1)

Evaluation
- Assess renal function, do urinalysis, where blood or protein in urine is coming from, acute or chronic,
         examine urine chemistries and FENa, and do renal imaging.
- Renal dysfunction/failure can be due to problems that are:
    o Pre-renal – blood flow
    o Intrinsic/parenchymal – within the glomerulus, tubules-interstitium, or vascular system
    o Post-renal – obstruction to outflow of urine
- GFR = (UCr*V)/PCr = Creatinine (Cr) clearance


Urinalysis
- Dipstick:
    o pH (5.2-5.4) – if > 7.0, UTI; if > 5.5 & acidotic, renal tubular acidosis
    o Glucose (0) – hyperglycemia, or Fanconi‟s S. (PCT cannot reabsorb)
    o Protein/SSA (< 150mg/day) – see below
    o Blood (0) – if it LOOKS like blood its probably NOT renal; a small tea or cola-colored amount is
         probably renal tubular dysfunction
    o Ketones (0) – acetoacetic acid and -hydroxy-butyric acid = (Diabetic) Ketoacidosis
    o Specific gravity (1.006-1.036) – correlates with osmolality of SMALL particles (Na+, K+, Cl-,
         NH3, salts)
    o Leukocyte esterase (0) – WBC metabolite = infex
    o Nitrite (0) – byproduct of urea splitting organisms = UTI
    o Urobilinogen (0) – hepatocellular
    o Bilirubin (0) – conjugated, must be very high levels before appears in urine = hepatobiliary
         obstruction or hemolysis

Glomerular vs. Non-glomerular Bleeding
- If it LOOKS like blood its probably NOT renal; a small tea or cola-colored amount is probably renal
          tubular dysfunction (repeat from above)

Proteinurias
- Glomerular: measured by excess albumin in urine
- Tubular: measured by level of small molecular weight proteins in urine, using SSA; also marked with
         2-microglobulin
- Overflow:
    o So much protein, can‟t filter it all
    o Excess Ig light chains, which are toxic to glomeruli and tubules = MM
- Dipstick vs. SSA:
    o Dipstick is sensitive to albumin only = glomerular problem
    o If excess protein is not albumin, must do an SSA (Sulfa salicylic acid) to detect small MW
         proteins
- Macro vs. micro:
    o Macroproteinuria/-albuminuria = if have 3.5g of albumin (normal <20mg) in urine
    o Microalbuminuria = <300mg, but still more than usual = prognostic indicator of renal injury
         (diabetes, HTN)




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Sediments
- Cells = WBCs, RBCs, epithelials
- Casts – formed by the Tam Horsfoll proteins from epithelial cells, and catches things flowing tubules
    o Hyaline => if in abundance, low flow rate
    o Cellular => WBCs, epithelials, RBCs (pathognomonic for glomerulonephritis)
    o Granular => released by degenerating cells, intrinsic renal failure
- Crystals – tumor lysis syndrome, or rhabdomyolysis (from damage)
- Bacteria – gram (-) rods

Acute vs. Chronic
- Notice onset, if there was prodrome or toxic injury
- Watch how BUN/creatinine levels change over time, patterns in urinalysis
- Trends in urine chemistry tests
- What is the trend of the patient? Getting worse?

Chemistries
- Especially fractional excretion of sodium = FENa
    o Proportion of Na+ filtered at glomerulus that is not reabsorbed, but excreted
    o Prerenal disease – FENa will be < 1%
    o Intrinsic renal disease – increased
    o FENa = (UNa*PCr)/(PNa*UCr)*100

Imaging Choices
- U/S – size and symmetry, obstructions or masses, test of choice
- IVP – anatomy, calyces; IV contrast
- CT – parenchyma, tumors
- MRI – thrombosis, vasculature/MRA (not used much)
- Nuclear scan – kidney function (glomerular uptake and tubular excretion); use Tc
- Angiography – vascular anatomy (renal artery stenosis), definition; IV contrast

Urinalysis (4)

3 Main Components
1.   Physical Exam
     o Color
              a. Normal is pale to dark yellow
              b. Dark yellow, amber, orange = bilirubin, pyridium, Rifampin
              c. Pink or red = RBCs, Hgb, Mgb, porphyrins, beets, azo dyes
              d. Brown to black = MetHgb, homogentisic acid, melanin
     o Appearance
              a. Normal is clear
              b. Cloudy = cells, crystals, bacteria, crystals, mucus
     o Specific gravity = density
              a. Normal = 1.001-1.035 (1.015-1.025)
              b. > 1.035 = glucose, protein, or dye in urine
              c. measuring urine osmolality is more accurate than SG, since determined only by
                 number of solute particles present
2.   Chemical Exam – see below
3.   Microscopic Exam – see below




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Chemicals and Significance
- pH (4.5-7)
     o Acidic = high protein diet, acidosis, and K+ depletion
     o Alkaline = vegetarian diet, alkalosis, and urease-producing bacteria
- Protein (40-80mg/day) – pathological causes
     o Glomerular disease (>3.5g/day)
     o Tubular disorders (<1.5 to 2g/day)
     o MM (light chain Ig‟s)
     o Pre-eclampsia => proteinuria in 3rd trimester
     o Microalbuminuria => albumin 30-300 mg/24h
     o Injury to glomerular filtration barrier
     o Predicts nephropathy
     o Protein determination is most important indicator or renal disease
     o Proteinuria from benign causes is transient and disappears after underlying cause is
           removed
- Glucose (~0)
     o DM
     o Glycosuria (normal plasma glucose) – Fanconi‟s S.
- Ketone bodies (0)
     o = Acetone, acetoacetic acid,  hydroxybutyric acid
     o Diabetic ketoacidosis, starvation, excess CHO loss
- Blood (0)
     o Hematuria (RBCs) – injured capillary bed along urinary system
     o Hemoglobinuria (Hgb) – transfusion reaction, hemolytic anemia, severe burns, infex, strenuous
           exercise
     o Myoglobinuria – muscle trauma, convulsions, muscle wasting, extensive exertion
- Bilirubin (0)
     o Metabolite of Hgb
     o Hepatobiliary disease, cause of jaundice
- Urobilinogen (<1mg/dL)
     o Bile pigment metabolite of Hgb from bacteria in intestine
     o Liver disease, hemolytic disorders
     o Absent in biliary obstruction
- Nitrite (0)
     o Metabolite of nitrate by bacteria
     o Rapid for UTI
- Leukocyte esterase (0)
     o Intact and lysed leukocytes
     o UTI

Sediments on Microscopic Exam
- RBCs
    o More than an occasional is abnormal
    o Deformed is possible glomerular pathology
- WBCs (< 5/hpf)
    o Increased neutrophils in urine = pyuria
    o Bacterial => pyelonephritis, cystitis, prostatitis, urethritis
    o Nonbacterial => glomerulonephritis, lupus nephritis
    o >1% eosinophils in urine is significant = drug-induced acute interstitial nephritis
- Epithelial cells – tubular damage in renal failure, tubular necrosis
    o Squamous cells
               o From lining of vagina, lower urethras



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              o Large cells with much cytoplasm and central nucleus
              o Specimen contamination
    o     Transitional cells
              o From lining of renal pelvis, bladder, and upper urethras
              o Smaller cells
              o Seldom pathological; if are, check for carcinoma
    o     Renal tubular cells
              o Most significant
              o Round, slightly large than WBC, with eccentric nucleus
              o In tubular necrosis, pyelonephritis, toxic reaction, graft rejection, GN, general viral
              o With lipid = oval fat bodies, in nephrotic syndromes
- Casts
     o    Acellular – hyaline and granular can be present in health and disease, after exercise or
          stress; with proteinuria, unless it disappears within 24 hrs, it is significant
               o Hyaline
               o Granular
               o Waxy – CRF
               o Fatty – nephrotic syndrome
               o Pigment -- hemolysis
     o Cellular – WBC, RBC, epithelial
- Bacteria
- Yeast – Candida albicans; DM, vaginal moniliasis
- Parasites – Trichomonas vaginalis, ova of Schistosoma haematobium and pinworm
- Spermatozoa – after sex or nocturnal emissions
- Crystals
     o In acid urine (urates and calcium oxalate normal):
               o Cystine
               o Tyrosine – protein metabolite, in urine of tissue degeneration/necrosis (liver
                   diseases)
               o Leucine – same as above
               o Bilirubin – obstructive jaundice
               o Cholesterol – nephrotic syndrome
               o Sulfonamide – dehydrated patients on sulfonamide
               o Tylenol
     o Alkaline (phosphates, calcium carbonates, ammonium urates normal):
Please make a note….
o GN => variable proteinuria, RBC casts, >70% dysmorphic RBCs
o Nephrotic syndrome => heavy proteinuria (>3.5g/day), fatty casts, oval fat bodies
o Pyelonephritis => mild proteinuria, increased WBCs, few RBCs, WBC casts, bacteria
o Acute Interstitial Nephritis => mild proteinuria, neutrophils, eosinophils, RBCs, WBC casts
o Acute Tubular Necrosis => mild proteinuria, tubular epithelial cells, muddy brown granular
     casts, epithelial cell casts
o Hyaline and granular casts in all above

BABY, BABY
Congenital Anomalies…(9)

Development
- Kidneys and testes form close to each other – kidneys ascend, testes descend
- Anomalies occur at kidney or along ureter




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Malformations
Renal Agenesis
- Absence of one or more kidneys

Hypoplasia
- Failure of kidney to develop to normal size and reduced number of pyramids
- Usually unilateral

Ectopic Kidney
- Malposition of kidneys just above pelvic brim
- May cause kinking of Ureters and infex

Horseshoe Kidney
- Fusion of lower poles of kidneys together
- Rare if upper poles fuse, or one upper and one lower

Cystic Diseases
Simple Cysts
- Single or multiple cysts in cortex 2-5cm with smooth walls filled with clear fluid
- Usually asymptomatic

Familial Nephronophthisis (Medullary Cystic Disease)
- Group of disorders with cysts in medulla and cortical atrophy
- Unexplained CRF in children

PKD
Adult
- AD inheritance, 1/1000
- Asymptomatic until >40yo
- Back pain, bilateral abdominal masses, proteinuria, hematuria, HTN, progressive RF
- 40% with polycystic liver disease
- 20% with cerebral berry aneurysms --> subarachnoid hemorrhage and death (5-10% of deaths)
- 20% with MVP (females)
- Adjacent nephrons are compressed by cysts and are atrophic
- 1/3 die from HTN, 1/3 from RF, 1/5 from infex

Childhood
- Rare, AR
- CT shows dilated collecting tubules perpendicular to cortical surface
- Related to liver cysts and congenital hepatic fibrosis

Hereditary Nephritis…
HN
- Not common, not important

Alport’s Syndrome
- X-linked
- Defective collagen synthesis
- + mental retardation; GN, nerve deafness, lens dislocation, cataracts

Fabry‟s Disease
- Lysosomal storage disease resulting in ceramide accumulation, in glomeruli and tubules




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ACID-BASE DISORDERS (25)
Kidney & Homeostasis
1. Secretes H+ at PCT, LOH, CT via Na+-H+ antiporter
2. Buffers H+ with HPO4- and NH4+ intralumenally
3. Reabsorbs filtered HCO3-
Regulated by:
- Extracellular pH
- Effective Circulating volume depletion
- Plasma [K+] => Na+/H+-K+ antiporter on capillary side of renal epithelial cell

4 Primary Disorders:
(Check flow chart in notes!)

Metabolic-…
(Change in [HCO3-] is primary)
1. Metabolic Alkalosis
 [HCO3-], pH (EC and IC)
- Due to: H+ loss (GI, GU, transcellularly) and exogenous base (citrate)
- Compensate via hypoventilation --> pCO2 --> EC pH

2. Metabolic Acidosis
 [HCO3-], pH (EC)
- Due to:
 acid production
     o Lactic acidosis
     o Ketoacidosis
     o Salicylates => toxic range > 40mg/dL; + respiratory center --> respiratory alkalosis
 acid excretion
     o Renal failure
     o Type 1 (distal) RTA (Renal-tubular acidosis) = impaired H+-ATPase pump
     o Type 4 RTA = hyporeninemic hypoaldosteronism
 base excretion
     o Diarrhea, type 2 (proximal) RTA
- Compensate via hyperventilation --> pCO2 --> EC pH
- Normal anion gap = HARDUP
- Increased anion gap = AMPLESUDS


Respiratory-…
(change in pCO2 is primary)
3. Respiratory Acidosis
pH, pCO2
- Due to: impaired gas exchange, impaired ventilatory pump, and CNS inhibition
- Compensate via  [HCO3-]

4. Respiratory Alkalosis
pH, pCO2
- Due to: increased respiratory drive
- Compensate via  [HCO3-]




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Diagnosis
- H&P
- Check electrolytes, other labs
- Which disorder with underlying disorder?
- Simple or complex?



DISORDERS OF WATER BALANCE
Osmoregulation – Disorders (14)
- Too much water => hypoNa+
- Too little water => hyperNa+
- Too much Na+ => edema
- Too little Na+ => volume depletion
- Posm~2XNa+

Water Balance/Osmolality/Na+
- Balance between H2O intake and H2O excretion
- Give salt only => Na+ in ECF and hence plasma => fluid from ICF to ECF
- Give H2O only => ECF volume increases/plasma Na + decreases => increase ICF by way of H2O
         movement in
- Give NS = increases ECF only

Regulation
Osmoregulation
- Via plasma osmolality
- Balance between H2O intake and H2O excretion

Volume Regulation
- Via perfusion
- Balance between Na+ intake and Na+ excretion

Regulators
RAA
Renin converts AT-ogen to ATI, ACE converts ATI to ATII (vasoconstricts, Na+ retention), ATII to
         Aldosterone
- Renin release is triggered by decreased perfusion to the kidney, peripheral baroreceptors, and decreased
         Cl- to macula densa of JGA
- Aldosterone causes retention of Na+ and excretion of K+ in CT (on luminal side), vasoconstriction,
         and Na+ reabsorption in PCT
     o Also enhances the Na+/K+ ATPase on basolateral side to get into/out of circulatory system
ANP
- Secreted inreto atrial stretch
- Vasodilates (natriuresis, water diuresis) and closes Na+ conductance channels (opposes above)

ADH
- Released inreto osmoreceptor stimulation in hypothalamus
- Determines H2O excretion/retention at collecting tubules
- In conjunction with thirst receptor stimulation to preserve the circulating volume




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-Natremias

Hyponatremia
- NOT too little salt, but too much H2O
- Causes:  ECV (CHF), thiazide diuretics, SIADH, advanced RF, Hypothyroidism, cortisol deficiency,
          primary polydipsia
     o Defect in suppression of ADH would not allow compensatory excretion of H2O, and remaining
          hypoNa+
     o Low CO of CHF stimulates RAA, which increases ADH (=non-osmotic ADH stimulation),
          which causes H2O retention and hypoNa+ (prognostic indicator of severity of the disease)
     o CHF and the RAA also increases thirst and H2O ingestion
     o SIADH (Syndrome of Inappropriate ADH) => from neuropsychiatric causes, drugs, ectopic
          neoplasm, post-op, pulmonary diseases
     o A reset osmostat, which is more sensitive than normal
- Diagnose via plasma and urine osmolality, and urine [Na +]
- Treat via H2O restriction, isotonic saline, hormone replacement, or nothing, depending on cause


Hypernatremia
- Due to unreplaced water loss (insensible, urinary, GI), or hypertonic NaCl or NaHCO3
- Usually protected via thirst mechanisms

Polyuria
= 3L/day of urine output
- Either due to problems with high [Na+] in filtrate, or unresponsiveness to ADH
- Central or nephrogenic DI, or primary polydipsia

Brain Volume and Osmolality
- Must maintain ICF, especially in brain, which is very restricted in its vault
- Brain generates osmolytes as protective = Na+, K+, inositol, glutamine, taurine
- Slow process, so acute situations are only ones requiring treatment, to alleviate neurological symptoms --
         (< 0.5 mEq/L/hr)


AGENTS FOR RENAL CONSERVATION OF H2O (10, aka “24”)
See Prachi‟s charts….

EDEMATOUS STATES
Disorders (15)

Formation
- Edema = expansion of ISF (interstitial fluid) volume

Capillary/Hemodynamic
- From the vascular space to interstitium
- Increased capillary hydrostatic pressure

Renal Na+ Retention
- Baroreceptors sense decreased CO or ECV--> decreases Na+ and hence H2O excretion
- H2O then expands ECF volume and into interstitium



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- OR, primary renal dysfunction => glomerular disease, or (mostly) in advanced renal failure

So, edema develops from:
     o Increased hydrostatic pressure => CHF, cirrhosis, renal disease, DVT, pulmonary edema,
        vasodilators
     o Decreased oncotic pressure => nephrotic syndrome, hepatic disease (not a major factor)
     o Increased capillary permeability => allergies, sepsis, burns, cytokines
     o Lymphatic obstruction or interstitial oncotic pressure => nodal enlargement

Disorders
Renal Disease/Failure
-  GFR -->  hydrostatic pressure --> can‟t modulate Na+ reabsorption, so  retention and edema

Nephrotic Syndrome
- Increase in hydrostatic pressure (vascular filling and inappropriate Na reabsorption)
- Decreased colloid oncotic pressure

CHF
- Decreased left ventricular function -->  SV -->  LV end diastolic pressure -->  pulmonary pressure
         and edema
- Decreased renal perfusion -->  RAA --> ADH (you know the rest)…

Cirrhosis
- Via:
     o Post-sinusoidal obstruction => increased hydrostatic pressure and ascites
     o Splanchnic vasodilation and AV shunting => hypotensive, decreased renal perfusion, increased
         neuronal reflexes --> Na+ and H2O retention…; spider angiomas and Caput Medusa
     o Decreased albumin synthesis => decrease serum oncotic pressure

Treatment (in combo with what follows)…
- Treat underlying cause, then diuretics
- Diuretics reach site of action via a protein (albumin), so hypoalbuminemia patients can be resistant
- Can cause hypoK+ and hypoMg2+

Diuretics
1. OSMOTICS
    o PCT and dLOH
    o Mannitol
2. CARBONIC ANHYDRASE INHIBITORS
    o PCT (most, 65-70% of Na+ reabsorption) – makes it weak
    o Acetazolomide (Diamox)
3. LOOP BLOCKERS
    o Medullary of thick aLOH (25%)
    o Competes for Cl- on Na-K-Cl transporter
    o Blumetanide, Ethacrynic Acid, Furosemide (Lasix), and Torsemide (Demadex)
    o Most potent – use in most edematous
4. THIAZIDES
    o DCT (3-8%)
    o Competes for Cl- on Na-Cl cotransporter (synergistic with loop diuretics)
    o Chlorthiazide, metolazone
5. K+-SPARING DIURETICS
    o CT‟s
    o Close Na+ conductance channels, and hence spares K+ through its channels
    o Spironolactone, amiloride, triamterene
    o Beware of hyperK+


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VASCULAR DISEASE
Pathology of HTN (16,17)

Essential
Etiology unknown; imbalance between:
- Peripheral resistance (humoral/neural constrictors/dilators, local)
     o Sympathetic activity
     o Increased CO
- CO (blood volume, heart rate, contractility)
     o Via increased blood volume from increased Na + reabsorption
- Renal function
- Na+ homeostasis (aldosterone)


Secondary
Etiology
- 5% Renal disease = acute/chronic GN, chronic pyelonephritis, PKD, renal artery stenosis, thrombosis,
         vasculitis
- 1% Endocrine disease = Cushing‟s S., PCC, thyrotoxicosis, acromegaly, Conn‟s S, BCP‟s, Liddle‟s S.
         (pseudohyperaldosteronism), GRA
- 3% Pill HTN
- COA, PAN


Kidney:
- RAA => angiotensin (SNS & vasoconstriction), aldosterone (Na+ & H2O retention = Na+ homeostasis)
- ADH => increase H2O reabsorption
- ANP (from heart) => inhibits Na+ reabsorption
- Renal vasodepressors (Pg‟s) are anti-HTN


Benign HTN/BNS (Benign Nephrosclerosis)
- GCK macro; hyaline arteriolosclerosis & fibroelastic hyperplasia/elastosis on micro
- Slowly rising BP over period of years, asymptomatic or if severe => HA, tachycardia, epistaxis, blurred
         vision, confusion/coma
- Die from: CHF, CAD/MI, CRF, CVA
- Prognosis depends on severity

Malignant HTN/MNS
- “Flea bitten” kidney on macro; fibrinoid necrosis & hyperplastic change (arteriolitis) on micro
- May progress to necrotizing glomerulitis
- Sustained diastolic > 120 associated with S/S is MHTN and medical emergency
- Increase in intracranial pressure => HA, N/V, visual impariment
- May be triggered by DIC
- Die from: RF, HF, or cerebral hemorrhage
- Prognosis if untreated = mortality 90%




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Renal HTN-Clinical (18)

1o HTN
Blah, blah…


2o HTN
- Na+ regulation by kidney is major determinant in HTN
- Salt-Sensitive HTN = low renin, high [Na +]i (elderly and African-American)
- Renin-Dependant HTN = JGA perfusion, RAA
- Goldblatt kidney = effects of clipping 1 or both kidneys on renin & ATII
      o Clip one kidney =>  renin & AII on unclipped side,  on clipped side
      o Clip both kidneys =>  renin & ATII
      o Have one kidney, clip it =>  renin & ATII


Reno-Vascular HTN
Pathophysiology
- Fibromuscular Dysplasia (~1/3) => no FMHx, < 25yo, white female
- Atherosclerotic (~2/3) => diffuse vascular disease, > 50 yo, cigarettes
- Abrupt, MHTN,  in function inreto ACEIs/ARBs

Diagnosis
- Captopril Renal scan => stimulated scintigraphy --> fall in GFR on affected side = (+)
- Gold Standard = Arteriography
         o High risk for refractory high BP
         o Diagnostic for lesion, route for therapy/stenting
         o Invasive, costly, dye nephropathy, embolism…

Management
- Resistance to therapy except ACE-I/ARB‟s



DISORDERS OF K+ BALANCE
K+ Homeostasis (19)

Renal/Extrarenal
- Cellular uptake depends on: insulin, EPI, plasma [K+]
- Urinary excretion depends on: aldosterone, distal Na + and H2O, plasma [K+]

HyperK+ Causes
- Exogenous K+
- Impaired cell entry
- Increased cell release
- Reduced urinary excretion
** HyperK+ cannot exist in the absence of impairment in urinary excretion

HyperK+ Treatment
- Stabilize cellular membranes with IV calcium



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- K+ redistribution: insulin and glucose, -adrenergic agonists, NaHCO3
- K+ removal: diuretics, dialysis, cation exchange resin

HypoK+
- Redistribution
- GI losses (diarrhea, vomiting, nasogastric suctioning)
- Urinary losses

Renal Potassium Wasting
- Via: diuretics, vomiting/diarrhea (normotensive) -- 1o mineralocorticoid excess, 2o hyperaldosteronism,
          renal tubular acidosis, renal artery stenosis (hypertensive)
- S/S of hypoK+ = weakness, polydipsia, polyuria, ECG changes
- Treatment of hypoK+ => treat underlying disorder, K+-sparing diuretics, K+ replacement

GLOMERULAR DISEASE

Pathology (5,6)

Pathogenesis of Diseases
1o Glomerulonephritis:
- Immune => immune complex, anti-GBM Ab‟s, and CMI

CPC (Clinico-Pathologic Correlation)
- Extent of glomerular injury = diffuse/focal (kidney) and segmental/global (glomerulus)
- Nephritis = hematuria, HTN
- Nephrosis = heavy proteinuria, hyperlipidemia, edema
- Combined

Acute Nephritic Syndrome:
- ACUTE DIFFUSE PGN
      o Granular deposits (“lumpy bumpy humps”) on immunofluorescence

- RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS (RPGN) aka. Crescentic GN
       o Linear deposits on immunofluorescence; crescents in glomerulus (serious)
       o GOODPASTURE’S SYNDROME – hemoptysis, hematuria


Nephrotic Syndrome:
Highly Selective Proteinuria
-
Poorly Selective Proteinuria
- Severe GBM injury --> loss of higher MW proteins
- --> hypoproteinemia, hyperlipidemia

- LIPOID NEPHROSIS aka. Nil Disease
       o Most common cause of NS in children
       o Fusion of foot processes of glomerular epithelial cells due to unknown etiology
       o Good prognosis
       o
- MEMBRANOUS GLOMERULONEPHRITIS (MGN) aka. Membranous Nephropathy



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                            RENAL/URINARY MIDTERM REVIEW


        o   Most common cause in adults
        o   Early subepithelial/epimembranous
        o   Late intramembranous
        o   Poorly selective proteinuria
        o   “Spikes” and “domes”

      o
- FSG
- AMYLOIDOSIS


Nephritic-Nephrotic Combo:
- MEMBRANOPROLIFERATIVE GN (MPGN) aka. Mesangio-Capillary GN (MCGN),
Hypocomplementemic GN
    o “ Double contour” or “tram-track” morphology


- IgA NEPHROPATHY aka Berger‟s Disease

- FOCAL PROLIFERATIVE GN (FPGN) aka. “Zo‟s Disease”


Glomerulopathy Secondary to Systemic Disease
- LUPUS NEPHRITIS (secondary to systemic disease)
    o wire loops
    o females
    o renal failure

- KIMMELSTIEL-WILSON DISEASE/DIABETIC NEPHROPATHY (secondary to systemic disease)
      o Excess glucose --> nodular deposits in GBM (= Nodular Glomerulosclerosis)
      o Thickened BM
      o #1 in causing chronic renal disease

Adults (7,8)

Pathophysiology of Proteinuria


Evaluation of Patient


Glomerulonephritis – Pathologically
- Circulating Immune Complexes, Circulating Ab to native or planted glomerular Ag, “Other”
- Nephrotic => noninflammatory => injury to epithelium minimal (FSGS), immune complex subepithelium
         (Membranous), GBM deposition disease (Amyloid, Paraproteins)
- Nephritic => inflammatory => anti-GBM Ab‟s, immune complex (PIGN, SLE)

Syndromes and Causes:
- ACUTE NEPHRITIC SYNDROME
      o Acute post-infectious (Strep) GM
      o Systemic, idiopathic
      o Lupus, diabetes


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                                RENAL/URINARY MIDTERM REVIEW


        o What to look for:
- RAPIDLY PROGRESSIVE GM
- MINIMAL URINARY ABNORMALITIES
        o IgA is most common glomerulonephropathy in world
- CHRONIC GM
- NEPHROTIC SYNDROME
        o Heavy proteinuria
        o Via systemic: Lupus,
        o Idiopathic: minimal change/old term, membranous GN (look for cancer), FSGS
        o Edema, hyperlipidemia, …
- IgA NEPHROPATHY
- DIABETIC NP – microalbumin, use ACEI, no IVP…,

HepC & GN

Diagnosis
- Biopsy
- CBC, Chemistries, UA, ESR, ANA, Anti-DNA, C3, C4….



RENAL FAILURE
Pathology (20,21)

ATN/ARF
Etiology
- Toxic form =>
- Ischemic form =>

Morphology

Clinical


CRF
- CRF refers to function, whereas ESRD refers to morphology

Causes of ESRD
- Chronic GN and HTNephrosclerosis => GCK that are symmetrical with fine granules
- Chronic interstitial nephritis (chronic pyelonephritis) => GCK that is assymetrical with large, irregular
         granules with depressed scars
- Polycystic kidney disease and chronic diabetic nephropathy (most common cause)

Ca2+ and PO4- Metabolism
- “Trade-off Hypothesis” = kidney is gone,

Clinical
- Anemia due to decreased erythropoietin (inhibited by uremia) => dysfunction of cells and increased infex
- VitD(3) is absent
- Uremic Osteodystrophy =




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                               RENAL/URINARY MIDTERM REVIEW


Azotemic/Uremic Syndromes
= increase BUN and creatinine levels, due to:
- Pre-renal = hypoperfusion -->
- Renal =
- Post-Renal =
- Uremia is toxic EVERYwhere in the body

Clinical - Acute (22,23)

Definition
= Abrupt decline in renal fxn, leading to retention of nitrogenous wastes and the loss of fluid and
         electrolyte homeostasis
- SIRS (Systemic Inflammatory Reaction Syndrome), MOF (Multiple Organ Failure)
Clinical
- Nonoliguric – from nephrotoxic ARF…
- Oliguric = < 400cc/day, from tubular necrosis…
- Anuric

Etiologies
Prerenal Azotemia or Ischemic ARF
- Structural lesions
- Volume depletion
- Reduced effect arterial volume – hepatic, sepsis…
- Drugs – NSAIDs, ACEIs, diuretics
         o Via: reduction in renal perfusion and alteration of renal hemodynamics

ATN (differential with above)
- Ischemic – generalized or localized reduction in renal blood flow (sepsis…)
- Nephrotoxic -- drugs causing direct tubular toxicity and that alter intrarenal hemodynamics, hemolytic-
         uremic syndrome, etc.
- Causes

Risk Factors
- Diabetes, age, myeloma, hyper Ca2+
- Hospital-acquired: ATN>AIN>…

Pathophysiology
- Nephronal
        o Vascular – vasoconstriction, decreased permeability
        o Tubular – backleak (into interstitial space), obstruction


Diagnosis
DDx
- ARF, oliguria, azotemia
- Prerenal => kidney healthy, low perfusion, low filtration
- Renal => GN, tubular necrosis, renal infarction…
         o Tubular necrosis (TN)= tubular cells died
                  o Ischemia (50%)
                  o Toxins (35%)
         o Interstitial nephritis (10%)
         o Acute GN (5%)
- Postrenal => secondary to obstruction


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                              RENAL/URINARY MIDTERM REVIEW



Urinalysis
- Prerenal – bland sediment
- ATN – RTE‟s, granular casts
- IN – WBC casts
- -- granular cast
-
Imaging
- KUB, IVP, CT, AGRAM, Nuclear Scan, U/S, Biopsy

Course/Management
- Initiation Phase
- Maintenance Phase
- Recovery Phase/
 Management
Modalities and what to avoid….

Clinical – Chronic (26,27)
- Renal Osteodystrophy => therapy with PO4- binders, vitD, treating metabolic acidosis

Renal Adaptation --> Loss of Function
Anemia
Renal Osteodystrophy
Common causes of ESRD in US:


Glomerular HTN/Hypertrophy


S/S
- Uremia (clinical) = skin, neurologic, GI, renal osteodystrophy, hematologic, anemia/bleeding tendency
    o Hiccups

Progressive CRF

ESRD


Slowing Progression
- Control BP…


Therapy
Progressive CRF
- MDRDS, Epogen, Calcitrol, acidosis, acquired cystic disease
- Nutritional therapy: MDRDS, keep 0.7-0.8g protein/day (well-nourished) and 1.1-1.2 in malnourished,
          treat lipid abnormalities

ESRD
- HD => conventional/high flux
- PD – CAPD
- Transplant


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                                RENAL/URINARY MIDTERM REVIEW



Dialysis




TUBULOINTERSTITIAL DISEASE
Pathology (12)

UTI
- Very common, M:F = 1:8
- 108 organisms/mL in urine
- Ascending --> VUR (vesicoureteral reflux)
- Hematogenous


Acute Pyelonephritis
- microabscesses
          o Pyonephrosis, perinephritic abscess
          o Necrotizing Papillitis
- tends to reoccur

Chronic Pyelonephritis
- Morphology = scarred and contracted (GCK),
- Pathophysiology -- 2 types:
        o Obstructive --
        o Reflux nephropathy-assoc.
- Complications = CRF, malignant HTN, ESRD (End-Stage Renal Disease),

Features of…
Tuberculosis of the Urinary Tract
- Hemorrhage => hematuria (in lungs => hemoptysis)
- Diagnose with urine culture for M. tuberculosis

Drug-Induced Pyelonephritis (Hypersensitivity)
-

Analgesic Nephritis
- Phenacetin
- Papillary necrosis
- prone to tranisitional cell carcinoma

Urate Nephropathy
- From treatment of lymphomas = high uric acid in blood

Hypercalcemia/Nephrocalcinosis
- Bone conditions (MM)
- HyperPTH, vitD intox…

Myeloma Kidney
- Bence Jones Proteinuria




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                                RENAL/URINARY MIDTERM REVIEW




Clinical (13)

Syndromes

Urinary Findings:
- Inflammation – WBC‟s and casts
- Toxics – epithelial and granular casts
- Chronics – bland, + glomerular proteinuria

Etiologies


Mechanisms
Susceptibility
- concentration gradients, cyp450‟s, free radicals

Analgesic
- Phenacetin-Aspirin metabolites => Pg inhibition, hexose-monophosphate shunt inhibition

Allergic
- T-cell mediated
- nonoliguric, fever, rash, eosinophilia(-uria)
- „cillins, Cephalosporins, NSAIDs, anticonvulsants, cimetidine…
- Tx = D/C above, steroids (?)

Obstruction
- Intratubular via myeloma, tumor lysis, drug precipitation
- In collecting system via calculi, tumors, retroperitoneal fibrosis, prostatic disease
- Leads to proximal tubule dilation, decrease GFR, glomerular vasoconstriction


Drugs for UTI’s (11, aka “28”)
See Prachi‟s charts!!

Sulfonamides
Oral Absorbable

Poorly Absorbable

Topicals


Resistance


Combos




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                     RENAL/URINARY MIDTERM REVIEW


Sulfas and H2O


(Fluoro)Quinolones

Antiseptics and Analgesics




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