Tubular & Interstitial Diseases

Question 1

What are the common features of Acute Tubular Necrosis

Answer 1

*acute decline in GFR,

*oliguria/anuria,

*serum BUN & Creatinine increased

Acute renal failure due to ischemic & toxic causes

Question 2

What are the 3 phases seen in Acute Tubular Necrosis (ATN) and what is seen in each phase

Answer 2

**Initiation phase (36 Hrs): Acute decrease in GFR to very low levels Rapid increase in serum creatinine & BUN

**Maintenance phase: -plateau of serum creatinine & BUN - Lasts for days to 3 weeks (oliguria) - Uremic symptoms, fluid overload, metabolic acidosis, hyperkalemia….dialysis

**Recovery phase: • Tubular function is restored • Increasing GFR • Increase urine volume • Gradual decrease in creatinine & BUN

Question 3

What is the laboratory,physical, and urinary finding of ATN

Answer 3

Urinary findings: • Muddy brown granular casts • Epithelial cells casts • Free epithelial cells • Proteinuria (mild) • Microscopic hematuria (mild) • No pyuria

laboratory findings: • Elevated serum Creatinine & BUN • Metabolic acidosis ( low HC03 ) • Hyperkalemia • Hyperphosphatemia • Anemia ( decrease erythropoietin )

Physical exam findings: - Hypotension - Low urine output ( oliguria / anuria ) - Uremic signs ( pericardial friction rub; confusion)

Question 4

what is seen in the patchy ischemic insuly of ATN?

Answer 4

• Hypotension
• Vasodilatory (septic shock)systemic infection
• Hemorrhagic shock: gastrointestinal bleeding
• Hypovolemic shock: vomiting, diarrhea

Question 5

What causes the diffuse Nephrotoxic insult in ATN?

Answer 5

*Exogenous: Aminoglycosides and Contrast media “CT/cardiac cath”

Endogenous: Hemoglobinuria and myoglobinuria

Question 6

What are the common features of Tubulointerstitial Nephritis

Answer 6

• Group of diseases characterized by interstitial inflammation, edema,/ fibrosis and normal glomeruli

• Tubular dysfunction:
- Impaired urinary concentration (polyuria, nocturia)

• Salt wasting ( hyponatremia )
• Metabolic acidosis ( decrease ability to excrete acid)
• No significant proteinuria or hematuria

Question 7

What causes acute and chronic Tubulointerstitial nephritis

Answer 7

• Acute: - Drugs (71%) (antibiotics) - Infection (15%) - Idiopathic (8%) - Sarcoidosis (1%)
• Chronic: - Infection (pyelonephritis) - Analgesic abuse (ASA, Tylenol) - Urate nephropathy

Question 8

What is the clincial presentation of Acute Drug Induced Interstitial Nephritis

Answer 8

• Onset usually 2 weeks after start medication

or

• 3-5 days if second exposure
• Symptoms & Signs: ( allergic – type reaction) - Fever (27%) - Rash (15%) - Eosinophilia (23%) - Triad of all (10%) or - ARF / oliguria - Asymptomatic

(first exposure)

Question 9

What are the urine and blood test results of Acute Drug Induced Interstitial Nephritis ?

Answer 9

*Urine microscopy: Eosinophils Sterile pyuria WBC casts Proteinuria (mild)

** Blood Tests: Increased BUN & Creatinine Increased eosinophils count Tubular dysfunction: High K, low HCO3

Question 10

What are the two pathways of Acute pyelonephritis

Answer 10

1- Bloodstream: seeding of kidney from distant source bacterial endocarditis, septicemia)

2- Ascending infection from lower urinary tract ( most common)

Question 11

What are the clinical manifestations and major complications of Acute pyelonephritis ?

Answer 11

• Fever • Dysuria • Flank pain • Nausea, vomiting • Costovertebral angle tenderness

**Complications: - Papillary necrosis - Pyonephrosis - Perinephric abscess

Question 12

What are the lab findinds of Acute Pyelonephritis

Answer 12

• Elevated WBC
• Pyuria, bacteruria,
• WBC casts
• Elevated BUN, Creatinine (volume depletion)

Question 13

What are the common features of Chronic Pyelonephritis?

Answer 13

• Recurrent or persistent renal infection
• Chronic tubulointerstitial nephritis
• Associated with progressive renal scarring
• Decline renal function…end-stage renal disease
• Occurs in patients with anatomical abnormalities

Question 14

What are the two major forms chronic Pyelonephritis?

Answer 14

1- Chronic obstructive pyelonephritis: Posterior urethral valves Kidney stones
2- Reflux nephropathy ( more common): Vesicoureteral reflux

Question 15

What is the clinical course of Chronic Pyelonephritis?

Answer 15

• Reflux pyelonephritis…silent onset….patient present
late in course of disease

• Renal insufficiency & hypertension • Proteinuria (mild) / significant with FSGS

**Gross: • VUR – preferential scarring & calyceal dilatation at poles • Obstructive – diffuse dilatation of calyces & scarring

• Microscopic: tubular atrophy, chronic interstitial inflammation, fibrosis in cortex and medulla
• FSGS

Question 16

How does Papillary Necrosis occur in pyelonephritis?

Answer 16

• Interstitial inflammation compress medullary
vasculature –> ischemia & papillary necrosis

• Treat underlying infection..(IV antibiotics)

Question 17

How does Obstructive Uropathy & Hydronephrosis occur?

Answer 17

• Dilatation of renal pelvis & calyces

As a result of continued glomerular filtration, but unable to be excreted due to obstruction..

• Diffuses back in to renal interstitium
• High pressure in pelvis is transmitted through collecting tubules into renal cortex…causing renal atrophy
• Renal function fully recovered if relieved fast
• Irreversible damage & renal failure if obstruction not relieved by 2-3 weeks

Question 18

What are the common stones in Nephrolithiasis?

Answer 18

1- Calcium containing - Calcium oxalate - Calcium phosphate

2- Struvite (Mg/Ammonium phosphate)

3- Uric acid

4- Cystine

Question 19

What is the clinical presentation of Nephrolithiasis?

Answer 19

• Silent if remain in renal pelvis
• Symptomatic if stone passes into ureters:

1- Renal colic: abrupt onset of flank pain radiatingto groin ( intermittent )

Nausea, vomiting, gross or microscopic hematuria (ulceration of urothelium)

2- Superimposed UTI – urinary stasis, trauma

3- Hydronephrosis due to obstruction of ureter

Question 20

How to prevent Nephrolithiasis?

Answer 20

• Decreasing urinary concentration of the
causing substances:

• Increased fluid intake (2L/day)
• Low sodium diet..decrease urinary calcium excretion CA reabsorbed in PCT with Na)
• Alkalinization of urine to (increase solubility of uric acid)