Ryan: Tubulointerstital Disease
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| What are the different types of tubulointerstitial disease? | Acute interstitial nephritis
Chronic interstitial nephritis
Acute tubular necrosis
Renal tubular acidosis
Multiple myeloma
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| List the general features of tubulointerstitial disease. | Proteinuria <1g/day
Anemia
Acidosis
Hypertension
WBCs and WBC casts on UA
Na and K abnormalities
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| List the general features of glomerular disease. | Proteinuria >3-3.5 g/day
Anemia is uncommon
Acidosis is uncommon
Hypertension
Oval fat bodies on UA
May see low Na
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| Acute interstitial nephritis (AIN) is also known as what? | Drug-induced hypersensitivity
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| What may be seen on UA? | Eosinophils, RBCs, WBCs, and WBC casts
NO RBC casts or fat bodies
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| Which drugs normally cause AIN? | Antibiotics
NSAIDS
Cimetidine
Thiazides
Allopurinol
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| What infections can cause AIN? | CMV
Legionella
Leptospiosis
Streptococcus
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| What clinical features will you see in a pt with AIN? | Rash
Fever
Azotemia (RF)
Malaise
Arthalgias
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| How soon after starting a new medication can these symptoms be seen? | 7-10 days after starting a new medication
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| What would you expect to see in a pts lab? | Eosinophilia
Elevated sed rate
Low C3&C4
WBCs and WBC casts
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| What stain is associated with AIN? | *Hansel's stain*
---BUZZWORD---
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| Which antibiotics most commonly cause AIN? | Beta-lactams
TMP/SMX (sulfa)
Ripfampin
Fluoroquinolones (rarely in kids)
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| What is the classic triad of AIN? | Fever
Rash
Eosinophils
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| What is this response related to? | No clue, not related to dose or duration
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| How long do you have to be taking NSAIDs before you start to see symptoms? | Several months
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| Why might the AIN triad not occur? | Anti-inflammatory drugs block the inflammatory response
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| What systemic diseases can cause AIN? | Sarcoidosis
SLE
Any infection (pyelonephritis)
Transplant rejection (drugs)
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| Tx of AIN | STOP THE DRUG!!!
Usually brings about an improvement of renal fxn
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| Chronic Interstitial Nephritis (CIN) | Chronic condition involving fibrosis of the interstitium and tubular destruction
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| What pts should this be on your DDx for? | Hx of frequent pain who present with proteinuria & elevated creatintine
Glucosuria with normal serum glucose
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| Check for _____ in kids | *lead toxicity*
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| What drug class may be responsible? | NSAIDs
Can cause acute or chronic IN
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| Name the post renal causes of CIN. | Chronic Obstructive Uropathy (urethral reflux)
Chronic Pyelonephritis
Chronic Renal Lithiasis
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| List the other causes of CIN | Medications
Post acute Tubular Necrosis
Autoimmune- Sjogren's syndrome
Raditaion
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| The hallmark of CIN | **Sterile Pyuria**
Inflammatory response to something
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| Clinical features of CIN | Usually asymptomatic
Anemia
Acidosis RTA
Minimal Proteinuria
Hypertension
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| Tx of CIN | BP control is the MOST IMPORTANT
ACEI/ARB are DoC
Anemia control
Acidosis control
Phosphorus control
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| Do you give a pt with CIN pyuria antibiotics? | NO
Not unless there is bacteria present
It's inflammatory, NOT an infxn
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| Acute Tubular Necrosis (ATN) | Most common RENAL ARF
Necrosis due to microthrombi
Frequently due to prolonged hypotension and augmentation of the immune system from sepsis.
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| Causes of ATN | Sepsis
Drugs (NSAIDs)
Post-operative-post CABG
Pancreatitis
Prolonged and Untreated prerenal conditions
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| Clinical features of ATN | Oliguric or non-oliguric
Azotemia
Elevations in serum Creatinine may not reflect the degree of renal dysfxn
Acidosis/hyperkalemia
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| ATN labs | Uosm <350, Una >40, FeNa >2
Plasma BUN/Cr <10-15
Ucr/Pcr <20
**Muddy brown casts on Urine Sed.**
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| Tx of ATN | Treat underlying condition
Dopamine doesn't work
ANP doesn't work
High dose Loops: limited
Dialysis MAY increase survival
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| Rental tubular acidosis (RTA) | Met. acidosis usually caused by a defect in renal tubular fxn (genetic)
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| How many types of RTA exist? | 3 types:
1 proximal (type 2)
2 distal (types 1 & 4)
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| What does the anion gap look like in RTA? | Normal gap metabolic acidosis
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| Relate RTA types with serum K | Type 1: Low K
Type 2: Normal L
Type 3: High K
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| Type 2 RTAs | Mechanism similar to acetazolamide
(decreased HCO3 reabsorption in the proximal tubule)
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| Causes Type 2 RTA in children | Fanconi Syndrome
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| Fanconi syndrome | Rare disorder of tubule fxn
Results in excess glucose, HCO3, phosphates, uric acid, K, Na, and some amino acids in the urine
May be hereditary
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| Etiologies of Type 2 RTA | Drugs
Heavy Metals
Disorders or protein, carbs, or amino acid metabolism
Multiple myeloma (adults)
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| Type 4 RTA | Affects Na/K-H exchange in the DCT
Similar to spirnolactone
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| Common etiologies of Type 4 RTA in kids | Obstructive uropathy
Interstitial renal dz
Multicystic dysplastic kidneys
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| Etiologies of Type 4 RTA | Type 1 pseudoaldosteronism
Diabetic nephropathy
21-hydroxylase deficiency
Renal transplant
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| RTA Type 4 Tx | Tx aimed at treatingthe primary dz
Try to give HCO3 but MUST restrict K
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| Type 1 RTA | Distal defect in H secretion
Pts become acidotic and hypokalemic
Commonly causes renal stones
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| How do children with Type 1 RTA present? | Commonly with failure to thrive
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| Etiologies of Type 1 RTA | Amphotericin B
Toluene
Lithium
SLE
Sjogren's Syndrome
Chronic active hepatitis
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| Multiple Myeloma | Blood cancer in which plasma cells grow uncontrollably, usually in the bone marrow
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| Associated bone lesions | Cause structural damage and/or fractures from overproduction of myeloma cells
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| Why is it referred to as Multiple Myeloma? | Because 90% of patients have multiple bone lesions
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| Causes of renal failure in MM | Cast nephropathy
Light chain deposition dz
Primary amyloidosis
Hypercalcemia
Renal tubular dysfunction
Volume depletion
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| Myeloma Kidney mechanisms | Intracellular cast formation
Direct tubular toxicity by light chains
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| Cast nephropathy | Most common pathological Dx on renal biopsy in MM
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| Light chains bind with this | Tamm-Horsfall Mucoprotein
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| Where is the Tamm-Horsfall mucoprotein secreted? | From tubular cells in the ascending loop on Henle
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| This will worsen cast nephropathy | Dehydration
Due to decreased flow and increase in [light chain]
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| Light chain deposition disease | Most commonly presents with both renal insufficiency and nephrotic syndrome
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| Which Ig id responsible? | Kappa Ig
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| What takes up/metabolizes the light chains? | Macrophages
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| Amyloidosis | Usually due to lambda light chains
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| What stain is used for amyloidosis? | **Congo Red**
Beta-pleated
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| Why does renal failure develop? | From tubular injury
Also presents as nephrotic syndrome
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| Hypercalcemia in MM | Occurs from bone reabsorption
15% of pts with MM
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| Contributes to renal failure by... | Renal vasoconstriction
Leads to intratubular calcium deposition.
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| Acquired Fanconi syndrome | Light chains cause tubular dysfunction w/o renal insufficiency
Mostly kappa light chains
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| Light chains are resistant to ___ and form ___ | Degradation
Crystals
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| Two ways tubular damage is caused | Light chain toxic effects
Indirectly from the release of intracellular lysosomal enzymes
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| MM lab findings | Elevated BUN and Creatinine
Hypercalcemia, uricemia
Low anion gap
UA shows NO protein
Elevations in the gamma fraction-Bence-Jones Protein
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| Tx of renal failure in MM | Hydration with IV fluids
Tx of hypercalcemia (Loops)
Tx of myeloma (steroids)
Possible plasmapheresis
Dialysis
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| ***MM Buzzwords*** | Chronin back pain
Males >50
African-American
Hepatosplenomegaly
Cardiomyopathy
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