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Flashcards in Renal Deck (229)
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Approach to patient with kidney issue

Laboratory testing:
• Serum Creatinine & Urea Nitrogen
• Creatinine clearance (Estimated GFR)
• Urinalysis with microscopic examination
• Urine Electrolytes and Osmolality
• Spot Urine Protein and Creatinine ratio
• 24 hours Urine Collection
• Assessing Urine Output
-Oliguria (400cc/day)

History and Physical examination

• Kidney Imaging (U/S, Doppler, Nuclear scan, MRI, Angiogram)

Invasive testing:
• Kidney Biopsy


Indication for renal biopsy

- Acute kidney injury
- Nephrotic or nephritic syndrome
- Hematuria
- Systemic Disease
- Transplant Allograft

ONLY perform biopsy if:
- Cannot determine with less invasive procedure
- Suggestion of parenchymal disease
- Differential diagnosis includes diseases that have different treatments and courses


Serum creatinine as measurement of GFR

Non-protein waste product of skeletal muscle metabolism

15-25 mg/kg/day= proportional to muscle mass; Serum concentration dependent on:
- Excretion (glomerular filtration)
- Secretion into lumen

Changes in creatinine excretion have hyperbolic relationship with GFR:
- jump from 1 to 2 mg/dL--> 50% loss of nephrons


Conditions changing creatinine excretion:

Decreased creatinine: less muscle mass
- Hepatic cirrhosis
- Limb amputation
- Spinal cord injury
- Morbid obesity

Increased creatinine: more muscle mass or drugs:
• Influence of muscle mass
• Blocking proximal secretion
- cimetidine, trimethoprim, probenecid
• Interference with Jaffe rxn e.g. ketones, methanol, cephalosporins, isopropanol
(mass spectroscopy, HPLC et al)



Blood: strip detects peroxidase
- blood, myoglobin, free hemoglobin
Leukocyte alkaline esterase detects polys.
Nitrate: detected by a reaction with an azo dye
- presence suggests bacteria
Protein: depends on urine concentration.
- 1+ as significant as 3+
Specific gravity closely approximates osmolality
- If specific gravity is high then concentrating ability likely intact


Urinary sediment types



Indications for Renal Ultrasound

To quantify kidney size
To evaluate for hydronephrosis
To evaluate the perirenal space for abscess or hematoma
To screen for ADPKD (polycystic kidney disease)
To localize the kidney for invasive procedures
To evaluate for kidney vein thrombosis (doppler US)
To assess kidney blood flow (doppler US)


Indications for IV pyelography

IV contrast dye given- monitor kidney excretion

To assess renal size and contour
To investigate recurrent urinary tract infection
To detect and locate calculi
To evaluate suspected urinary tract obstruction
To evaluate the cause of hematuria


Indication for radionuclide studies

To quantify total kidney function and the contribution of each kidney
To evaluate kidney parenchymal integrity
To evaluate kidney infection or scar
To evaluate renovascular hypertension
Little benefit when the single kidney GFR is below 15 ml/min


Glomerular filtration agent (renal scan)

- Freely filtered by the glomerulus and is not reabsorbed
- To estimate GFR
- Technetium diethylenetriamine pentaacetic acid (99mTc-DPTA)


Tubular secretion agents (renal scan)

- Evaluate renal blood flow and function
- Plasma clearance
- Technetinum mercaptoaceyltriglycine (99mTc-MAG3)


Tubular fixation agents (renal scan)

- Bound to the tubules and delineates the contuor of functional renal tissue
- To assess cortical scarring from pyelonephritis and/or vesicoureteral reflux
- Technetium dimercaptosuccinate [99mTc-DMSA]


Indication for renal CT

To further evaluate a renal mass
To display calcification pattern in a mass
To delineate the extent of renal trauma
To guide percutaneous needle aspiration or biopsy
To diagnose adrenal causes for hypertension (50% of HTN is genetic, other causes linked to renal function)


Indication for renal MRI/MRA

• Diagnosing renovascular lesions
• To assess renal vein thrombosis
• Evaluation of potential living kidney donors and transplanted kidneys
• To evaluate suspected pheochromocytoma
• Delineating complex mass where CT is not definitive
• Staging kidney neoplasms, particularly in evaluating for renal vein or inferior venal caval extension of tumor


Indication for renal angiography

• Suspected artery lesions: atherosclerotic or fibrodysplatic stenoic lesions of the renal arteries, aneursysms, arteriovenous fistulae.
• Large vessel vasculitis
• Unexplained hematuria
• Kidney transplantation
• Diagnoses for renal vein thrombosis
• Complex or highly unusual renal masses or trauma etc

“Can be used for diagnostic or for therapeutic purposes”


Definition of Acute renal failure (ARF)

Acute loss of kidney function
- Typically connotes acute drop in GFR

Multiple definitions of this, typically based on changes in:
- Serum Creatinine
- Urine output

Other definitions of ARF:
1. Oliguria: <50cc UOP/day
3. Azotemia: elevated blood urea nitrogen (BUN ) without symptoms of uremia
4. Uremia: buildup of toxins that are cleared by the kidney. Most of these toxins are unknown.
** An elevated Urea level alone is NOT sufficient to diagnose uremia


Differential diagnosis of ARF

1. Prerenal causes
2. Intrinsic causes:
- Tubular necrosis
- Interstitial nephritis
- Acute glomerulonephritis
3. Postrenal causes


Pre-renal azotemia

Elevated nitrogen levels in blood NOT due to kidney damage
- Renal blood flow decreased--> decreased GFR--> decreased clearance of metabolites
- Kidney is intact and cells are not damaged
- Kidney avidly reabsorbs salt and water to try and preserve intravascular blood volume and renal blood flow.

- History of volume depletion
- Exam consistent with volume depletion
- Fractional Excretion of Na (FENa) < 1 %
- Urine Na < 20 mEq/L (low if kidney is Na avid, tubules intact)
- Urine Osm > 500 mOsm/L
- Increased BUN/Creatinine Ratio
- Bland urinalysis
- Ultimate Test: Give Fluid
- If immediate improvement, then it’s pre-renal


Hepato-renal syndrome

Advanced liver failure- toxins usually cleared by liver cause:
- Splanchnic vasodilatation
- Renal vasoconstriction
- Urine Looks Like Pre-Renal Azotemia
- Urine Na < 20mEq/L
- Bland UA
- Does not get better with saline


Post-renal obstruction

In patients with two functioning kidneys, both need to be effected to produce significant renal failure
- Urethral obstruction – most common
- Obstruction of a solitary kidney
- Bilateral ureteral obstruction

- Urethral obstruction
- Bladder neck obstruction (prostatic hypertrophy, bladder carcinoma, bladder infecion)
- Bilateral ureter obstruction:
1. Intraureteral:
- Sulfonamide, uric acid crystals, blood clots/stones
2. Extraureteral:
- tumor (cervix, prostate, endometriosis)
- Retroperitoneal fibrosis
- Ureteral ligation/edema due to pelvic operation


Diagnosis of post-renal obstruction

• Historic predisposition:
Benign Prostatic Hypertrophy
Abdominal malignancy
• Symptoms of obstruction:
Urinary frequency/urgency (suggesting urethral obstruction)
Patients with post-renal ARF do NOT need to be anuric. A partial obstruction may still lead to enough back-pressure to decreased kidney function

Urinalysis: bland sediment
Urine lytes: not helpful
Evidence of obstruction: renal U/S, abdominal CT


Acute tubular necrosis/ injury (ATN/ATI): types

Defined as sudden death of tubular cells (NOT glomerular cells)

There are two sub-categories of ATN:
1. Ischemic ATN: results from severe renal hypoperfusion. Ischemia results in death of susceptible tubular cells
2. Nephrotoxic ATN: injury secondary to substances that directly damage renal tubules, leading to cell death


Acute tubular necrosis: causes

- Septic shock
- Extensive trauma
- Massive hemorrhage
- Post-operative
- Pancreatitis
- Pregnancy- post-partum hemorrhage
- Transfusion reactions

- Radiocontrast media
- Antibiotics (aminoglycosides, amphotericin)
- Myoglobin (rhabdomyolysis)
- Hemoglobin
- Heavy metals (mercury, arsenic, lead, bismuth, uranium, etc.)
- Insecticides
- Chemotherapy
- Uric acid, calcium

* Need to hydrate patients when exposed to nephrotoxic substances to dilute toxicity


Acute tubular necrosis: Diagnosis

- History: prolonged hypotension, muscle crush, toxin exposure, drugs, coma, seizures

Urine sediment:
- granular casts on urinalysis
- Casts= mucoprotein secreted by renal tubule cells
--> decreased GFR--> increased accumulation of casts

Urine lytes:
- Na > 20 mEq/L or FENa> 1%

Pathology finding (rare to biopsy):
- Normal glomeruli
- Tubular epithelial cells flattened with pyknotic nuclei, swelling and necrosis of cells with sloughing into tubules
- Interstitium – edema with minimal cellular infiltrate


Acute interstitial nephritis: casues

Allergic reaction in kidney
Typically due to medications:


Acute interstitial nephritis: diagnosis

- Drug hypersensitivity
- Eosinophil > 10% in periphery

Urine WBCs with negative culture (no infection)
- Casts with no pyelonephritis
- No urinary obstruction/inflammation of kidneys on imaging

Gold standard diagnosis: kidney biopsy


Acute glomerulonephritis

Inflammation of glomeruli, typically auto-immune

Urine sediment:
- Dysmorphic RBCs
- RBC casts, WBC casts
- Proteinuria

Acute post-infectious glomerulonephritis
Autoimmune diseases:
- Polyarteritis nodosa
- Henoch-Schonlein purpura
- Goodpastures syndrome
ANCA vasculitis (most common cause in hospital)


Renal athero-emboli

Small atheromatous crystals flecking off arterial wall--> kidney
- After manipulation of arteries (post-embolization)
- Loss of kidney function after 1-2 weeks
- Urine bland, maybe eosinophilia
- PE may show emboli (fingertips)
- No specific treatment


Management of ARF

1. Pre-renal:
- replace fluid
- CHF: treat arrhythmias, inotropes, reduce load

2. Post-renal:
- Remove cause/bypass obstruction (EMERGENCY when creatinine begins to elevate)

3. Acute tubular necrosis:
- No interventions will improve renal function after onset of acute tubular necrosis


Supportive care of Acute Renal Failure

1. Intravascular volume (overloaded):
- low salt diet, water restriction
- diuretic use
2. Hyponatremia:
- restrict free water, avoid D5W in IVF????
3. Hyperkalemia:
- Renal diet, eliminate K/K-sparing diuretics
- K-binding ion exchange resin in colon
- Glucose/insulin, 50-100 mEq NaHCO3, albuterol, Ca-gluconate
4. Metabolic acidosis:
- Sodium bicarb to maintain HCO3 > 15
5. Hyperphosphatemia, hypermagnesemia, hypocalcemia
- Phosphate-binding agents
- Avoid milk
- Discontinue Mg-containing antacids (malox, mylanta)
- Ca-gluconate, Ca-carbonate