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