Renal Path Flashcards
1
Q
Pronephros
A
- Forms at begining and present until week 4 when it degrades.
- Not functional
2
Q
Mesanephros
A
- Functional from week 5 to 32-36 weeks.
- Ureteric bud comes off caudal end
3
Q
Ureteric Bud
A
- Comes off caudal end of mesenephros and works with metanephric mesenchyme to make definitive kidney.
- Ureters to Collecting duct are made from ureteric bud
4
Q
Metanephros
A
- Begins developing at week 5 and functional by week 32-36.
- Contains metanephric mesenchyme
5
Q
Metanephric mesenchyme
A
- Works with ureteric bud to form the definitive kidney.
- Forms proximal portion from DCT to glomerulus
6
Q
Horsehoe Kidney
A
- Fusion of inferior pole of kidney
- Gets stuck on IMA during ascent.
- Still functional and seen commonly in turners syndrome
7
Q
Multicystic Dysplastic Kidney
A
- Impaired communication between metanephric mesenchyme and ureteric bud leads to degradation of kidney.
- Cystic spaces with fibrotic stroma in betweem
- Most commonly unilateral. Contralateral kidney hypertrophies and picks up function.
8
Q
Potter sequence
A
- Oligo hydramnios leads to lung hypoplasia (Cause of death), facial deformities, and club feet/arms
- Can be caused by: Posterior urethral valves (Problem with wolfiian duct, bilateral renal agenesis, ARPKD
9
Q
Uretopelvic Junction
A
- Last portion to canalize and most commonly impaired.
- will lead to congenital hydronephrosis
10
Q
Ureters Anatomy
A
-Retroperitoneal structures that go under the uterine arteries and and ductus deferens
11
Q
Macula Densa
A
- Modified cells in association with DCT. In close aproximation with JG cells.
- Works to regulate renin secretion and constriction of afferent arteriole in response to changing Na/Cl concentrations.
12
Q
Fluid Compartments
A
- 60% body water, 40% normal tissue
- Of 60%, 2/3 is intracellular and 1/3 is extracellular
- Of extracellular, 3/4 is interstitial and 1/4 is plasma
- Measure plasma with radio-labeled albumin
- Normal osmolarity is 290 (approximately 2xNa)
13
Q
Glomerular Barrier
A
- Fenestrated endothelium is size barrier and prevents RBC from penetrating
- BM contains large quantities of heparan sulfate which is highly negatively charged. Proteins will be repeled (loss in nephrotic syndrome leads to proteinuria)
- Podocytes of bowman’s epithelial cells
14
Q
Substance Filtration
A
- Small polar molecules are completely filtered and must be reabsorbed
- Large proteins are not filtered
- Lipophilic substances (steroids, bilirubin) will be bound to almbumin and large proteins so won’t be filtered.
- If glucuronidation or sulfation leading to increased water solubility will increase ability to be filtered
15
Q
Renal Clearance
A
- The volume of fluid from which all of a substance has been cleared
- Renal excretion/plasma concentration
- Ux*V/Px
- If greater than GFR then net secretion
- Less than GFR net reabsorption
16
Q
GFR
A
- Meausured acurately with the celarance of inulin. Freely filtered by not secreted or resorbed
- Clinically done with creatinine
17
Q
Effective Renal Plasma Flow
A
- Calculated by PAH clearance
- All of PAH is secreted therefore plasma flow.
- At really high PAH concentrations transporter can be saturated and will no longer be accurate
18
Q
Renal Blood Flow
A
-Renal Plasma Flow/ (1-Hct)
19
Q
Filtration fraction
A
-GFR/RPF, normally 20%
20
Q
Filtered Load
A
GFR* plasma concentration
21
Q
Prostaglandins effect on filtration and GFR
A
- Cause dilation of afferent arteriole leading to increased RPF and Increase GFR with no change in filtration fraction.
- NSAIDs oppose this action and will decrease RPF and GFR
22
Q
Angiotensin 2 effect on filtration and GFR
A
- Preferentially constricts efferent arteriole leading to decreased RPF with increased GFR and increased FF.
- ACEI will inhibit this leading to an increase in RPF and decrease in GFR and FF. Given to “all diabetics” takes strain off kidneys
23
Q
Glucose Clearance
A
- Driven by Na/K symporter. Normally all glucose is reabsorbed, but demonstrates saturation kinetics
- at 160,g/dl there is the start of splay (some saturated) at 350mg/dl is complete saturation of receptors.
- Glucosuria will be seen from 160 onwards.
24
Q
Glycosuria of Pregnancy
A
- Increased blood volume leads to increased RPF and GFR which increases filtered load of glucose and saturates glucose transporters at lower glucose levels.
- Is normal and not pathalogic
25
Q
Amino Acid Clearance
A
-Saturation kinetics like glucose however rarely saturated
26
Q
Hartnup disease
A
- Congenital lack of neutral amino acid transporter leading to impaired tyrptophan reabsorption and absorption from the gut.
- Tryptophan makes niacin and lack of transporter will lead to lack of niacin and pellegra.
27
Q
Proximal Convuluted Tubule
A
- Reabsorption of almost everything. Reabsorbs all glucose, amino acids. Most HCO3, 2/3 Na and 2/3 H20
- Generates an isotonic urine (water follows Na)
- Generates NH3 to be used as buffer for acid in collecting duct
- Has CA, HCO3 reabsorbed and H+ secreted and complexes with HCO3 in urine. No net production of HCO3.
28
Q
Carbonic Anhydrase Inhibitors
A
- Prevent reabsorption of HCO3 leading to diuresis
- Also can cause slight metabolic acidosis
- Acetazolamide used to treat altitude sickness that is brought on by hyperventalaion induced metabolic alkalosis.
29
Q
PTH role in PCT
A
-Cause decrease in function of phosphate transporters.
Leads to phosphate excretion
30
Q
Ang II role in PCT
A
-Causes increase in Na/H antiporter leading to increased Na and bicarb reabsportion leading to increased tonicity of blood and increasd blood volume.
31
Q
Thin Descending limb of henle
A
-Impermiable to Na and flows down the corticomedullary gradient resulting in reabsortpion of water and concentration of urine
32
Q
Thick Ascending Limb
A
- Impermiable to water and dilutes the urine
- Na/K/2Cl pump reabsorbs these ions. Blocked by loop diuretics (ferosumide) (hypokalemia possible)
- Reabsorption of Ca and Mg occurs because of positive luminal membrane potential generated by K backleak
33
Q
Early DCT
A
- Na/Cl transporter, blocked by thiazides leads to reduced Na and Cl reabsorption
- Cl can be absorbed paracellularly
- Makes urine more hypotonic (impermiable to water)
34
Q
How Thiazides increase Ca reabsportion
A
-Blockage of Na/Cl channel means that all Na pumped out of cell with Na/K pump will then only be able to enter the cell from the basilar side in the Na/Ca exchanger. This leads to increased Na/Ca exchanger function and incresed Ca absorption.
35
Q
How Thiazides can be used in Nephrogenic DI
A
-Decresed Na/Cl reabsorption means there is more in the lumen. This is sensed by the JG aparatus as GFR that is too high. This will feedback to the afferent arteriole and cause constriction and reduction in GFR. Decreased GFR leads to decreased diuresis in the collecting Duct
36
Q
PTH effects on Early DCT
A
-Cause increased Ca absorption through Na/Ca exchanger
37
Q
Collecting Duct Principle Cell
A
- Mainly concerned with water and electrolye absorption
- Contains and inducable (aldosterone) Na channel.
- Contains aquaporins induced by V2 ADH receptors
- K+ leak channel that functions to secrete K with low intraluminal K concentrations
38
Q
Amilioride/Triamterene
A
-K sparing diuretcs that block the Na channel in the collecting duct. Decreased intracellular Na leads to decrease in Na/K pump and decreased K leak. Leading to K sparing properties
39
Q
Sprinolactone
A
-Blocks aldosterone receptor. Prevents protein synthesis of Na channel. Effects same as K sparing diuretcs
40
Q
ADH
A
- Gs receptor that puts aquaporins on luminal membrane leading to increased reabsorption of water.
- Urea follows water and will be reabsorbed too.
41
Q
Intercalated Cell
A
- Functions in acid base balance.
- CA splits H20 and CO2 to make HCO3 and H
- HCO3 is generated here and is free. Works to alkalanize plasma (HCO3 in PCT is not free and is complexed with H)
- Main channel is primary active trasport H pump that pumps hydrogen into the lumen.
- Pump is slowed if luminal pH drops. Therefore acid must be complexed with luminal substances to be buffered out.
- Phosphate can absorb H and NH3 (produced in PCT) can absorb H+ (more)
42
Q
Renal Tubular Acidosis I
A
- Dysfunction of H+ pump in intercalated cell leads to impaired HCO3 production and impaired H secretion
- Urine will have a high pH
- Fanconi’s syndrome
43
Q
Renal Tubular Acidosis II
A
- Impaired HCO3 production in PCT leads to decreased production and transfer into plasma.
- Increased urine pH predisposes to production of calcium phosphate renal stones
44
Q
TF/P
A
- Water is resorbed along the length of the PCT at the same rate as K and Na
- Substances that are resorbed more rapidly have a TF/P of less than 1 (glucose, AA, Phosphate, HCO3)
- Substances that are absorbed slower are above 1 (inulin, Cl, Urea, creatinine)
45
Q
JG Aparratus
A
- Consists of JG cells (granular cells) That are modifiec smooth muscle cells of the afferent arteriole that secrete renin.
- Macula Densa cells of the DCT that detect Na/Cl concentrations.
- Increased Na/Cl delivery means that GFR is too fast and signals through adenosine to cause constriction of the afferent arteriole to decrease RPF and GFR
- Decreased Na/Cl means GFR is too low signalling a release of renin that results in the preferential constriction of the efferent arteriole and increasing GFR and FF at a lower RPF
46
Q
RAAS
A
- Release of Renin from JG (Granular cells) is stimulated by decrease Na/Cl (macula densa), B1 SANS stimulation, decreased BP (decreaed RPF and decreasd GFR)
- Renin converts angiotensinogen to ang 1 which is converted to ang2 in lungs by ace.
47
Q
ACE
A
- Enzyme in lungs that activates ang I to ang 2
- Also degrades bradykinin, ACEI can induce massive angioedema and tongue swelling in some patients.
48
Q
Ang 2
A
- Main role is to increase BP
- Systemic effects on AT1 receptors cause vasoconstriction
- Causes preferential constriction of efferent arteriole which leads to increase FF and preserves GFR in the face of decreased RPF
- Causes release of aldosterone which will increase Na reabsorption and volume expansion. ADH is primarily concerned with osmolarity
- Causes release of ADH which acts through Gs receptors to place aquaporins in the collecting duct to increase water absorption. Mainly concerned with volume status
- Inhibits reflex bradychardia in baroreceptors of carotid sinus
- Increases Proximal Tubule Na/H activity. Increases Na, HCO3, and H20 reabsorption
- Stimulates thirst sensor in hypothalamus
49
Q
Aldosterone
A
- Mainly concerned with volume
- Functions to increase Na reabsoprtion in exchange for K and H.
- Excess leads to hypokalemic alkalosis
- Nuclear receptor that increases Na channel expression in collecting duct
50
Q
ANP
A
- Stimulated by stretch in the atria.
- Binds to receptor and increases intracellular cGMP and NO concentrations leading to vasodilation
- Increases GFR and decreases Renin
51
Q
ADH
A
- Mainly concerned with osmolarity
- Released in PP and causes aquaporin insertion in collecting duct.
52
Q
EPO
A
-Released from interstitial cells of peritubular capillary in response to hypoxia
53
Q
1 alpha hydroxylase
A
-Converts 25 vitamin D to 1,25 (Active form) in response to PTH.
54
Q
Potassium Homeostasis Transcellular shifts
A
- K exchanged for H ions in acid base disturbances
- K/Na pump brings in K under increased metabolic demand
- Short term is transcelllar shifts, long term is aldosterone
55
Q
Causes of internal shift
A
- Increase function of Na/K ATPase.
- Beta adrenergic stimulation, Insulin
- Alkalosis
- Hypo-osmolar state
56
Q
Causes of external shift
A
- Acidosis (exchange for H)
- Digitalis impairs Na/K pump
- Beta blockers
- Hyper-osmolar state
- Cell Lysis
- Insulin Resistance/deficency (DKA)
57
Q
K Regulation
A
- Long term is done by aldosterone by insertion of Na channel in collecting duct, more Na will be absorbed in the place of H and K. This leads to K loss and H loss
- Gut absorption can also regulate. Diahrrea loses K and HCO3. Only time when you will see a hypokalemic acidosis.
58
Q
Hypernatremia
A
- Stupor, Mental Status changes, Siezures, Coma
- Hypovolemic: Dilutional, from fluid loss
- Euvolemic: From DI. No response to ADH means less water reabsobed, aldosterone compensation.
- Hypervolemic: Aldosterone hypersecretion (Conn’s)
59
Q
Hyponatremia
A
- Stupor mental status changes, coma
- Hypovolemic: CHF/Renal Failure
- Euvolemic: SIADH
- Hypovolemic: Addisons or primary adrenal insuficency
60
Q
Hypokalemia
A
- U waves, flattene T waves, Arrythmia, Muscle weakness
- Diuretics, High aldosterone (conn syndrome)
61
Q
Hyperkalemia
A
- Peaked T waves, wide QRS, arrythmia, muscle weakness
- Renal Failure, Addisons disease (primary renal insufficency)
62
Q
Hypocalcemia
A
- Tetany, trosseau/chvotek’s, siezures
- Renal failure, post transfusion citrate, PTH removal
63
Q
Hypercalcemia
A
- Bone pain, abdominal pain and constipation, polyuria
- Cancer (squamous cell lung, breast, multiple myeloma)
- HyperPTH (MEN and primary)
- Thiazide diruetics also increase Ca
64
Q
Hypermagnesiumemia
A
- Interferes with Ca flow
- Bradycardia, weakness, hypotension, cardiac arrest, hypocalcemia.
- Renal failure
65
Q
Hypomagnessiumemia
A
-Tetany and arrythmias
66
Q
Hypophosphatemia
A
- Bone loss and osteomalacia
- HyperPTH, Vitamin D deficency
67
Q
Hyperphosphatemia
A
- Metastatic calcification, hypocalcemia, renal stones
- Renal failure or PTH failure
68
Q
Metabolic Acidosis
A
-Primary increase in acid leads to primary decrease in HCO3. Respiratory compensation via hyperventalation and decreased CO2
69
Q
High Anion Gap Metabolic Acidosis
A
- Caused by the introduction of non H+ acid
- MUDPILES
- Methanol, Uremia, DKA, Propylene Glycol, INH, Lactic acidosis, Ethylene glycol, Salicylate poisoning
70
Q
Normal Anion Gap Metabolic Acidosis
A
- Caused by impaired release of H+ or increased H+ production
- RTA
- Acetazolamide
- Diahrrea (loss of HCO3 and also K, will result in hypokalemia)
- Blockage of aldosterone (Addisons, spironolactone)
71
Q
Metabolic Alkalosis
A
- Loss of acid
- Vommiting (also lose K, severe hypokalmeia)
- Hyperaldosteronism (Conn’s syndrome)
- Loop Diuretics (contraction alkalosis) (ang 2 and aldosterone work to increase plasma volume and also increase HCO3 reabsorption, also less solute present to dilute out extra HCO3)
72
Q
Fanconi Syndrome
A
-Dysfunctional PCT leading to the loss of a number of solutes including glucose, AA, etc
73
Q
RBC Casts
A
- Glomerulonephritis
- Malignant HTN/Ischemia
74
Q
WBC Casts
A
- Pyelonephritis
- Acute graft rejection
75
Q
Ganular/Muddy Brown Casts
A
-Acute Tubular Necrosis
76
Q
Fatty/Ovoid Casts
A
Nephrotic Syndrome
77
Q
Waxy Casts
A
-Chronic Renal Failure, advanced renal disease
78
Q
Hyaline Casts
A
No specific finding. Can be seen in normal patients
79
Q
Nephrotic Syndrome
A
- Increased permiability to protein because of loss of filtration barrier
- Albuminuria
- Hypogammaglobulinemia: Loss Ab may predispose to infection
- Loss of ATIII leads to hypercoagulable state
- Hypercholesterolemia from liver induced protein production.
- Edema
80
Q
Minimal Change Disease
A
- Most common cause of nephrotic syndrome in kids
- Normal glomeruli on H and E but EM will show flattening and effacement of foot processes from epithelial cells
- Commonly presents following an illness and induced by cytokine mediated damage.
- May be seen with hodgkins lymphoma
- Tx with steroids usually has good response
81
Q
Focal Sclerosing Glomerulonephritis
A
- Most common cause in african americans and hispanics. Also in AIDS patients, heroin and sickle cell.
- EM will show podocyte effacement
- LM will show focal sclerotic lesions
- Does not respond to steroids.
- Commonly progresses to chronic renal failure
82
Q
Membranous Glomerulonephritis
A
- Most common cause of nephrotic syndrome in caucasians
- Deposition of immune complexes subepithelial causing a spike and dome appearance.
- Granular appearance on LM
- Associated with SLE, Hepatitis, Drugs, and solid tumors
83
Q
Membranoproliferative Glomerulonephritis Typ I
A
- Nephrotic Syndrome, can be nephritic syndrome
- Subendothelial deposits, associated with hepatitis B and C
- Mesangial cell proliferation causing BM splitting
84
Q
Membranoproliferative Glomerulonephritis Type 2
A
- Nephrotic Syndrome, can be nephritic syndrome
- Basement membrane deposits
- C3 nephritic factor, Ab that stabalizes C3 convertase leading to inflammation.
85
Q
Diabetic Glomerulonephritis
A
- NEG of BM leads to increased permiability and leakiness (micoalbuminuria)
- NEG of efferent arteriole leads to hyperfiltration injury
- Diuresis leads to decreaed Na/Cl delivered to macula densa and increase in renin releas by JG cells leading to further efferent arteriole constriction through ang 2
- Treatment with ACEI can reduce hyperfilration injury
- LM will show focal nodules of massive sclerosis with mesangial expansion
86
Q
Amyloidosis
A
- Amyloid deposition in BM leads to compromise of filtration function.
- Congo red stain
- AL associated with multiple myeloma
- AA associated with chronic inflammation (RA and TB)
87
Q
Nephritic Syndromes
A
- Inflammation in the glomerulus leading to peimiablilty of RBC and influx of inflammatory cells.
- RBC casts are characteristic
- Clinically will present with oliguria (tubular blockage), Fluid retention and HTN, Azotemia, Hematuria, edema
- Inflammation commonly causes reduction in C3 and C4 levels in the plasma and can be probed on BM
88
Q
Post Strep GN
A
- Most commonly occurs post impetigo skin infection with nephrogenic strains, consequence of M protein.
- Deposition of immune complexes (type 3) leading to C3 and C4 activation and inflammation predominantly neutrophils, C5 chemoatractant.
- Granular lumpy subenpithelial deposits on IF
- Serum will show positive ASO and decreased C3 and C4
89
Q
Rapidly Progressive GN
A
- Characterized by crescent formation from hyperfiltration and deposition of fibrin, macrophages, complement, etc.
- Rapidly fatal if not treated and can be cauesed by a number of different factors
90
Q
Goodpasteur’s
A
Type 2 hypersensitivity with anti-GBM Ab that recognize collagen four.
- Cause a linear IF
- Presents with hemoptysis and RPGN
91
Q
Diffuse Proliferative (lupus associated)
A
- Type 3 deposistion of immune comlpexes in the kidney (subepithelial) resulting in activation of complement and inflammmation
- Most common cause of death in lupus patients.
- Will see characteristic Wire Loops on LM
92
Q
Wegners Granulomatosus
A
- Necrotizing small vessel vasculitis that is characterized by granulomatous inflammation
- Presents with classic triad of Nasopharyngeal signs, Hemoptysis, and Nephritic Syndrome
- C-ANCA positive
93
Q
Microscopic Polyangiitis
A
- Small vessel necrotizing vasculitis
- P-ANCA positive. Distinguish between Churgg Strauss with presence of Neutrophils
94
Q
Churgg Strauss-
A
- Necrotizing small vessel vasculitis
- P-ANCA positive
- Pts have asthma and eosinophils and distinguishes from microscopic polyangiitis
95
Q
IgA Nephropathy
A
- IgA depsotion post URI in the Mesangium
- Activation of C3 and mesangial proliferation and hypercellularity
- Commonly assocaited with HSP
- Most common world wide
- Will be accumlaitve effect of waxing and waning with each mucosal pathogen
96
Q
Henoch-Sheolen Purpura
A
- IgA vasculitis with palpable purpura on extensor surfaces
- Most commonly presents in children as purpura and abdominal pain.
- Nephritic Syndrome is also commonly involved.
97
Q
Alports Syndrome
A
- X linked congential malformation of type 4 collagen leads to basement membrane splitting
- Causes nephritic syndrome, hearing loss, and sometimes vision loss.
- No immune complexes
98
Q
Nephrolithiasis
A
- Formation of stones in the kidney from decreased water or increased solute
- Treatment can always be increase hydration
- Causes colicky flank pain and may cause micropscopic hematuria
- Can cause obstruction leading to hyddronephrosis and post renal azotemis
- Can be a nidus for UTI
99
Q
Hydronephrosis
A
-Post renal obstrucion leading to backup of fluid and may cause pressure atrophy of renal parenchyma
100
Q
Calcium Oxalate
A
- Calcium stones are most common, form at acidid pH
- Hypercalcemia, hypercalcuria
- Oxalate from crohns disease and ethylene glycol
- Tx: Hydration, Thiazides (Ca sparing), Citrate (Ca chelator)
101
Q
Calcium Phosphate
A
- Form in alkaline urine (think of alk phos)
- Most commonly from elevated Ca
- Tx: hydration, thiazides, citrate
102
Q
AMP Ammonium, Magnesium, Phosphate
A
- Occur in the presence of infection with Proteus, Klebsiella, or less commonly staph
- Organisms split urea to generate ammonia and alkalanize the urine
- Causes staghorn caliculi that must be removed surgically
- Can be a nidus for serious pyelonephritis
103
Q
Uric Acid
A
- Radiolucent. Will not show up on X-Ray, only CT
- Less, common and seen in the face of acidic urine and elevated uric acid levels
- Uric acid in pts with gout or myelodysplastic syndromes (tumor lysis syndrome)
- Allopurinol in pts with gout. Alkalinize urine with K HCO3
104
Q
Tumor lysis syndrome
A
- Most commonly occurs in Leukemias or myelodysplastic syndromes
- Elevated uric acid causes stone formation and acute renal failure
- Stones and electrolyte abnormalities are halmarks (Hyperkalemia)
105
Q
Cystenine Stones
A
- Formed in patients with autosomal recessive defect in positively charged AA transporter (Lysine, orntihine, etc)
- Reccurent stones in children
- Treatment is fluids and alkalination of the urine.
106
Q
Renal Cell Carcinoma
A
- Tumor of proximal tubular cells. Most common primary renal tumor
- Biopsy will show sheets of cells with clear cytoplasm (glycogen)
- Caused by mutation in VHL TSG which acts as E3 ligase for HIF 1 alpha.
- Can be associated with VHL (Along with cerebellar hemangioblastomas)
- Also increased risk with smoking and obesity
- Spreads hematogenously to bone and lungs and carries a poor prognosis. If nodal involvment will invole retroperitoneal nodes.
- Most commonly presents with hematuria, flank pain, and flank mass.
- May also present with left sided vericocele
- Paraneoplastic syndromes: EPO release causing polycythemia (Budd-Chiari), ACTH (Cushings), PTHrP (Hypercalcemia), Renin (HTN)
107
Q
Wilms Tumor
A
- Composed of immature Blastema cells
- Sheets of small blue, primitive cells that may form primative glomeruli
- Most common tumor of palpable mass in young kids.
- Associated with WAGR (Wilms tumor, aniridia, genitourinary abnormalities, retardation)
- Beckwith-Wiedermann (Uniparental Disomy)- macroglossia, abdominal wall defects, gigantism. More common in IVF
108
Q
Transitional Cell Carcinoma
A
- Carcinoma arising from the lower urinary tract. Calyces, pelvis and downwards.
- Urothelial Cancer, most common in bladder
- Associated with exposure to carcinogens concentrated in urine. Smoking, dyes, cyclophosphamide, phenacetin.
- Field effect. Cancer in bladder suggests significant exposure of bladder to tertogen and high liklihood of many recurent cancers
109
Q
Squamous Cell Carcinoma of lower GI
A
-Rare and must occur in the face of squamous metaplasia from long term irritation (infections, stones, etc)
110
Q
Adenocarcinoma of Bladder
A
-Occurs from urachal remnant and is seen on the bladder roof.
111
Q
Angiomyolipoma
A
- Tuberous Sclerosis
- Hamartoma of blood vessels and adipose tissue
112
Q
Acute Pyelonephritis
A
- Infection of the renal parenchyma most commonly from ascending infection
- E Coli is most common in elderly
- Fever, Costovertebral tenderness, flank pain, maybe hematuria
- Fever important and can cause sepsis in elderly patients.
113
Q
Chronic Pyelonephritis
A
- Multiple bouts of acute pyelonephritis can lead to scarring of the kidney tubules
- Most commonly from VUR in children or chronic stones
- Thyroidization of the kidney when eosinophilic material is deposited inside the tubules and appears like thyroid follicles
114
Q
Interstitial Nephritis
A
- Drug induced inflammation, pyuria, and azoteima
- Eosinophils in urine are almost pathognemonic
- Presents with azotemia, hematuria and rash and tenderness.
- Most commonly with diuretics, sulfa drugs, penicilins, rifampin and NSAIDs
115
Q
Diffuse Cortical Necrosis
A
- Ischemic infarcts along the cortex of the kidney
- most commonly following DIC/vasoapasm
- Classically follwing septic shock or obstetric emergency (Abruptio placenta)
116
Q
Acute Tubular Necrosis
A
- Necrotic cell death of renal tubular cells results in granular muddy brown casts, oliguria with decreased GFR, HTN, Hyperkalemia, Acidosis
- Can be Ischemic of Toxic
- Toxins: Aminoglycosides, Radiocontrast, Myoglobin/hemoglobin
- Recovery can occur in 1-3 weeks. Recovery is characterized by oliguria and hyperkalmic acidosis
- Post recovery there is polyuria with risk of hypokalemia
117
Q
Pre-Renal Azotemia
A
- Decrease GFR and decrease RPF secondary to hypoprofusion.
- Systemic hypotension, thrmobosis, etc
- Functioning tubules will resorb BUN and secrete Cr leading to an elevated BUN:Cr ratio > 15
- FeNa < 1 and urine osmolarity > 500
118
Q
Post Renal Azotemia
A
- Obstruction (BPH, stone, etc) leads to backup of urine and increased hydrostatic pressure in bowmans space leading to decreased GFR and normal RPF.
- Can become hydronephrosis and atrophy.
- Shares characteristics of pre-renal and post renal azotemia
- BUN:Cr > 15 FeNa normally not too high and osmolarity of urine is somewhat normal.
119
Q
Intrarenal Azotemia
A
- Caused because of tubular death and ATN
- Dysfunctional tubules leads to blockage of flow and decreasd GFR, inabilty to resorb BUN, inability to concentrate urine and resorb Na.
- Serum BUN:Cr<15, oliguria, hyperkalemia, acidosis
120
Q
Chronic Renal Failure
A
- Most common causes are HTN and DM which cause hyperfiltration injury.
- Electrolye imbalances leading to hyperkalemia, acidosis
- Anemia due to failure of peritubular interstitial cells to secrete EPO
- Hypocalcemia and hyperphosphatemia due to impaired Ca resorbption, impaired phosphate excretion, and impaired vitamin D production
- Na and Water retention leading to CHF, Edema, HTN
- Uremia
- Dyslipidemia
121
Q
Uremia
A
- Elevated BUN and nitrogen containing compounds
- Platelet dysfunction, pericarditis, encephalopathy with asterixis
122
Q
Renal Osteodystrophy
A
- Subperiosteal osteoporosis due to renal failure
- Increased Ca loss in urine leads to elevated PTH and Ca reabsorption (Osteoporosis)
- Impaired 1 alpha hydroxylase leads to decreased Ca resorption and osteomalacia
- Impaired phosphate excretion leads to dystrophic calcifications and complexing of Ca-P in blood leading to decreased free Ca
123
Q
Liddle Syndrome
A
- Congenital defect in ubiquitan ligase that leads to increased ENaC levels in Collecting duct.
- Pseudohyperaldosteronism
- Elevated Na and water leading to hypertension
- Increased excretion of K and H leading to hypokalemic alkalosis
- Tx: with ENaC blockers: Amilioride, triamterene (K sparing)
- Serum renin will be high and aldosterone will be low. Therefore doesn’t respond to ACEI or spironolactone
124
Q
ADPKD
A
- Autosomal dominant defect in transmembrane Ca homeostasis and signalling proteins leading to cystic kidneys
- Usually appears in adulthood with progressive renal failure and pain. Hematuria, oliguria. Enlarged cystic kidneys on CT/ultrasound.
- Associated with Berry Anyeurisms (HTN also), Mitral prolapse, Heptic Cysts
125
Q
ARPKD
A
- Autosomal recessive verison that is characterized by in utero renal failure
- May lead to potter sequence if severe
- If survive patients have massive hepatic fibrosis leading to protal hypertension.
126
Q
Medullary Cystic Disease
A
- AD defect that leads to progressive interstitial fibrosis of the kidney parenchyma and cystic dilations in the medulla.
- Progressive renal insufficency with inabilty to concentrate urine.
- Shrunken kidneys on CT
