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97 Cards in this Set

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  • Back
Statistically, how does renal blood flow decrease as a person reaches age 80?
Statistically it decreases 1200 ml/minute to 600 ml/minute
Why might serum creatinine be normal but GFR be decreased?
As patients age, they loose muscle mass and are thus producing less creatinine, so even though the GFR is decreased and the creatinine should be proportionally increased, the decreased muscle mass masks the problem by causing an overall normal or lowered creatinine level.
How would you estimate creatinine clearance from a random creatinine level?
Creatinine clearance = 140 -
In diabetic patients with a compromised GFR and a normal creatinine level, would Metformin be recommended?
Must first test whether they have a normal GFR - most certain test is a 24 hour creatinine clearance urine test.

Creatinine clearance can be masked in an elderly patient with reduced muscle mass
How does tubular function change as one ages?
Proximal tubular function declines with age, including maximal excretion of p-aminohuppurate and maximal resorption of glucose.

Renal threshold for glucose decreases with age - less glycosurea in given level of blood glucose.
How are fluid and electrolyte balances affected by age?
The ability to conserve sodium loss in Na+ deprivation is impaired
Ability to excrete Na+ in response to increased Na+ load is impaired
Ability to excrete K+ is impaired partly due to decreased RAAS
Ca++ absorption in the gut is less due to decreased hydroxylation of active vitamin D, but tubular reabsorption not normally affected.
What are renal disease states associated with aging?
Renal vascular disorders
Acute glomerulonephritis
Nephrotic syndrome
Acute Renal Failure
Chronic Renal Failure
Urinary Tract Infections
What kinds of Urethral/Ureteral Obstructions are common in older patients?
Prostate - BPH, neoplasm

Pelvic tumors - ovarian, uterine

Urinary tract tumors



Urosepsis may also occur
If an asymptomatic patient has a positive urine culture, how should it be treated?
Watch the patient for UTI symptoms - do not treat until symptomatic, as people who are chronically infected have an even higher likelihood of developing ABx resistance

Also, treatment doesn't have a significant enough demonstrable effect.
What may increase the risk of urosepsis, particularly in older patients?
Post-renal problems
List some general categories of causes for acute interstitial nephritis.
List some general categories of causes for chronic tubulointerstitial disease.
Hereditary renal disease
Exogenous toxins
Metabolic toxins
Autoimmune disorders
Neoplastic disorders
What are some of the basic functional consequences of tubulointerstitial disease?
Reduced GFR - obliteration of microvasculature and obstruction of tubules
Hyperchloremic acidosis - reduced ammonia production, type 1 RTA, proximal bicarbonate wasting
Tubular proteinuria - failure of proximal tubule protein reabsorption
Polyuria - damage to medullary tubules and vasculature
Hyperkalemia - potassium defects including aldosterone resistance
Salt wasting - distal tubular damage with impaired sodium reabsorption
Fanconi syndrome - damage to proximal tubular reabsorption of glucose, amino acids, phosphate, bicarbonate
How do drugs and toxins cause tubulointerstitial nephritis?
May trigger an interstitial immunologic reaction, like acute hypersensitivity nephritis
What is a classic example of a drug that triggers an interstitial immunologic reaction (acute hypersensitivity nephritis)?
How might a drug like cyclosporine cause acute renal failure?
A potent immunosuppressive agent - can cause reduced renal blood flow, ischemia, and nephritis.
What are some examples of drugs and toxins which, down the line, may cause slow cumulative damage to renal tubules?
Lithium, cyclosporine, chinese herb nephropathy (those containing aristolochic acid)
What are the clinical S/S for acute drug-induced interstitial nephritis?
Start ~15 days after exposure

Fever, eosinophilia, rash, renal abnormalities (hematuria, mild proteinuria, leukocyturia, oliguria, elevated serum creatinine)
What are some of the most common drug culprits for acute drug-induced interstitial nephritis?
Sulfonamides, beta-lactams, vancomycin, quinolines, erythromycin, rifampin, NSAIDs, diuretics, anticonvulsants
What is the likely pathogenesis behind acute drug-induced interstitial nephritis?
Thought to be an idiosyncratic immune response that causes increased IgE in some patients, suggesting that late-phase reaction of IgE-mediated hypersensitivity may be involved.

Some cases suggest T cell-mediated delayed hypersensitivity reaction.
What are the typical symptoms of drug-induced acute interstitial nephritis?
Acute intrinsic renal failure

Mild-moderate proteinuria
What is the classic triad associated with drug-induced acute interstitial nephritis (in addition to acute renal failure)?

Skin Rash

Peripheral Blood Eosinophilia

(Only in 10% of patients, however)
What may be seen in the urine sediment of a patient with acute interstitial nephritis (drug induced)?
Often Pyuria (WBC, WBC casts)
RBC casts are RARE
How does one visualize the kidney problem in acute interstitial nephritis (drug induced)?
Renal ultrasound may show bilateral kidney enlargement

Biopsy is the gold standard - may not be needed if symptoms resolve after withdrawal of offending drug
How is drug-induced acute interstitial nephritis treated?
Remove and/or treat underlying cause

Supportive measures - correct fluid and electrolyte abnormalities, symptomatic treatment of rash, fever, pain
Consider corticosteroids - small studies have shown good improvement within 72 hours of starting treatment
What is analgesic nephropathy?
A form of chronic renal disease caused by excessive intake of analgesic mixtures and characterized morphologically by chronic tubulointerstitial nephritis and renal papillary necrosis.
What is the most common mixture of drugs causing analgesic nephropathy?
Aspirin, Caffeine, Acetaminophen, and Codeine

Requires regular consumption of large quantities of at least 2 antipyretics.

**Phenacetin (an analgesic that was withdrawn by the FDA) was the first drug noted to cause analgesic nephropathy**
What are the clinical S/S of analgesic nephropathy?
Inability to concentrate the urine
GI symptoms
UTI - 50% of cases
What are some treatments for analgesic nephropathy?
Screen at-risk patients
Discourage use of problematic medications
Quit using the medications and correct fluid/electrolyte imbalances, consider corticosteroids.
How do acetaminophen (and phenacetin) cause analgesic nephropathy (papillary necrosis)?
Renal cells are injured because the drugs deplete them of glutathione, and generate oxidative metabolites
How does aspirin cause analgesic nephropathy (papillary necrosis)?
Contributes by inhibiting the vasodilatory effects of prostaglandins, predisposing the papillae to ischemia
What are some non-drug causes of papillary necrosis?
Urinary tract obstruction
Sickle cell disease
Renal tuberculosis
Describe the distribution, time course, infection and calcification incidence, and overall effect on papillae in Diabetes Mellitus.
Male-to-Female 1:3
Time course - 10 years
Infection - 80%
Calcification is rare
Several papillae are affected, all of same stage
Describe the distribution, time course, infection and calcification incidence, and overall effect on papillae in Analgesic Nephropathy.
Male-to-Female ratio - 1:5
Time course - 7 years of drug abuse
Infection - 25%
Calcification is frequent
Almost all papillae are affected, at different stages of necrosis
Describe the distribution, time course, infection and calcification incidence, and overall effect on papillae in Sickle Cell disease.
Male-to-Female ratio - 1:1
Variable time course
Infection may occur, may not occur
Calcification is rare
Few papillae are affected
Describe the distribution, time course, infection and calcification incidence, and overall effect on papillae with Obstruction.
Male-to-Female ratio - 9:1
Variable time course
Infection - 90%
Calcification is frequent
Variable numbers of papillae are affected
What syndromes are included in NSAID nephropathy?
Acute renal failure
Acute hypersensitivity interstitial nephritis
Nephrotic syndrome (membranous nephropathy)

Occurs mostly in patients who have already had some renal compromise, and take NSAIDs regularly
May contribute to hyperkalemia in at-risk individuals
Describe the pathogenesis of NSAID nephropathy.
NSAIDs inhibit cyclooxygenase-dependent prostaglandin synthesis
The selective COX-2 inhibitors affect the kidneys because COX-2 is expressed in human kidneys

Inappropriate vasoconstriction and increased risk of renal ischemia are the potential outcomes

NSAIDs also directly impair potassium secretion in the distal nephron
How does Lithium affect the kidneys?
Induces tubular atrophy, interstitial fibrosis, tubular cysts, focal segmental glomerulosclerosis

Result: Chronic Renal Insufficiency

May also induce nephrogenic diabetes insipidis - renal resistance to ADH - causing polyuria and polydipsia
How is Lithium nephropathy prevented?
Regular renal function screenings in patients prescribed Lithium
Stop Lithium at the first sign of renal impairment and substitute another medication

CKD may still progress even without Lithium
What is Cystic Kidney Disease?
Cystic diseases are hereditary, developmental and acquired disorders

Important because they are fairly common, some forms are major causes of chronic kidney disease, and are important to differentiate from malignant tumors
Describe the epidemiology of Cystic Kidney Disease (adult).
Autosomal dominant
Results in large multicystic kidneys
1/400-1000 births
Caused by genetic mutations in chromosomes PKD1 and PKD2
What are the associated risks of cystic kidney disease?
Liver cysts
Berry aneurysm
What are the renal effects in cystic kidney disease?
Flank pain
Urinary tract infections
Renal calculi

Typically results in CKD between ages 40 and 60
What is the pathophysiology of cystic kidney disease?
Renal cysts expand through the years, ultimately destroying the renal parenchyma, inducing interstitial inflammation and fibrosis along the way

It is thought that mutations in proteins related to mechanosensation by tubular cilia and calcium flux result in abnormal growth/differentiation of tubular epithelial cells, leading do abnormal ECM, cell proliferation and fluid secretion = cyst!
What are some causes of tubulointerstitial nephritis?
Primary event in tubulointerstitium in absence of glomerular injury (proteinuria); In presence of tubular injury (WBC in urine)

Secondary to glomerular or vascular disease
What is the most common cause of tubulointerstitial nephritis?
Drug induced - acute TIN, chronic, analgesic nephropathy
What are some characteristics of acute tubulointerstitial nephritis?
Rash, Edema
Positive skin test
High IgE
Not dose related

Generalized interstitial edema by lymphocytes, plasma cells, macrophages, eosinophils
What are some clinical features of acute tubulointerstitial nephritis? Blood characteristics?
Clinically - fever, hematuria

Blood - Azotemia, eosinophilia
What are some features of urine in acute tubulointerstitial nephritis?

Negative urine culture
What are some characteristics of chronic tubulointerstitial nephritis?
Tubular atrophy
Mononuclear cells
What is a common cause of chronic tubulointerstitial nephritis?
Analgesic nephropathy
What kind of necrosis is caused in analgesic nephropathy?
Renal papillary necrosis - dose related (Acetaminophine, Aspirin, Caffeine, Codeine)
What are some clinical features of analgesic nephropathy?
Chronic renal failure

Increased risk of transitional cell carcinoma of the renal pelvis or bladder
What are some characteristics of acute pyelonephritis histologically?
Acute neutrophilic exudate within tubules and interstitial inflammation

Tubules are filled with acute inflammatory cells with surrounding congestion
What is acute pyelonephritis?
Acute inflammation of the pelvis, tubules, interstitium

Usually caused by ascending bacterial infection from the urinary bladder
What are some predisposing factors for acute pyelonephritis?
Urinary obstruction (prostatic hypertrophy, uterine prolapse)
Vesicoureteral reflux
Neurological deficits
What is the most common causative organism behind acute pyelonephritis?
Escherichia coli
What are the gross morphological characteristics of a kidney with acute pyelonephritis?
Kidney has discreet patchy abscess

Yellow streaks (pus) extend from the pelvis to cortex on cross sections

LM - inflammatory infiltrate within lumen and interstitium, edema in interstitium
What are some causes of Chronic Pyelonephritis?
Vesico ureteric reflux
Lower Urinary Tract obstruction
Prostatic Hyperplasia
Renal Calculi
What are some histological / morphological characteristics of chronic pyelonephritis?
Tubular atrophy
Dilated tubules
Eosinophilic material is there, resembling thyroid tissue
Chronic inflammation
What are some morphological characteristics of kidneys with chronic pyelonephritis?
Blunt calyx
Uneven scarring
Calyceal deformities
What are some causes for acute renal failure?
Renal - acute tubular necrosis (toxic, ischemic - 50% of ARF), severe glomerular diseases, RPGN, acute (drug induced) interstitial nephritis

Prerenal - Ischemia

Postrenal azotemia - urinary obstruction
What are some causes of renal azotemia (intrinsic renal failure)?
Acute tubular necrosis (ischemia, toxins)
Diseases of small vessels and glomeruli - GN and vasculitis, HUS, TPP, malignant hypertension
Diseases of large renal vessels - renal artery thrombosis
Acute diseases of tubulointerstitium
What is the cause of acute tubular necrosis? What is happening pathologically and clinically?
It is caused by ischemic or toxic injury, or as part of tubulointerstitial nephritis

Pathology - destruction of tubular epithelial cells

Clinically - acute loss of renal function, oliguria and elevation of BUN and creatinine
Describe the pathogenesis of acute tubular necrosis.
Increased afferent arteriolar resistance

Tubular obstruction

Backleak of filtrate

Decreased permeability of glomerular filtration membrane
Is acute tubular necrosis permanent?
No, it is reversible - renal tubular epithelial cells have the capacity to regenerate - as long as there is intact basement membrane
How does tubular cell injury result in acute tubular necrosis?
Ischemia causes detachment of tubular cells
Renal tubular cell casts obstruct the lumen
Increase in intratubular pressure
Decreased GFR
How does loss of polarity occur in Acute Tubular Necrosis?
Na+K+ATPase enzyme moves from basolateral surface to luminal side

Increase in Na+ delivery to proximal tubules

Feedback to glomeruli produces vasoconstriction and release of Renin-Angiotensin

Overall results in a lower GFR
What are some microscopic features of acute tubular necrosis?
Focal epithelial necrosis

Tubulorrhexis (detachment of tubular cells from basement membrane)

Loss of proximal tubular brush border

Hyaline casts

Sloughing of epithelial cells

Interstitial edema
Why are tubular epithelial cells so susceptible to ischemia?
They have high metabolic rates, and are in a vulnerable position?
In toxic acute tubular necrosis, where is the necrosis localized? What are the most common causes?
Necrosis is prominent in the proximal tubules, while the tubular basement membrane is spared

Caused by drugs, amino glycosides, heavy metals, mushroom poisoning, pesticide, myoglobin, CCl4
In ischemic acute tubular necrosis where is the necrosis localized? What are the most common causes?
Necrosis - patchy, proximal tubules and ascending thick limb of the loop of Henle

Casts are in the DCT and collecting duct

Causes include severe hemorrhage, hypotension, dehydration
Describe childhood polycystic kidney disease.
Autosomal recessive
Progressive and fatal
BIlateral enlarged kidneys
May be associated with hepatic cysts
Describe adult polycystic kidney disease.
Autosomal dominant
Symptoms appear by age 40, presenting with renal insufficiency, intermittent hematuria, hypertension


Associated with Berry aneurysm, liver cysts
What are some histological / microscopic characteristics of autosomal dominant (adult) polycystic kidney disease?
Cyst filled with desquamated cells and fluid

Surrounding tissue exhibits interstitial fibrosis and scattered chronic inflammatory cells
Describe a simple cyst (polycystic kidney disease).
They may present as a single cyst or many. Confined to the cortex.

Present with hematuria and pain
How does a cyst in polycystic kidney disease (adult) present radiographically?
Smooth contour

In ultrasound - Fluid-filled
How do you approach a patient with unilateral flank pain and hematuria?
History and Physical where appropriate
Urine analysis
Imaging if appropriate, as needed
What are the different renal imaging modalities and relative costs?
Plain X-Ray - KUB, IVP, flat plate ($100)
Computed Tomography (CT) - with or without contrast ($1000)
Magnetic Resonance Imaging - with or without contrast ($2000)
Ultrasound (USN) - imaging or vascular ($500)
Nuclear medicine - flow, function, reflux ($1000)
What are some risks associated with IV iodine contrast?
Renal toxicity
Acute renal injury (acute tubular necrosis)
Prevention is best policy - serum creatinine > 1.5; GFR < 60 ml/1.73m^3; Avoid NSAIDs, risk factors like DM, MM;

Avoid volume depletion - hydrate pre- and post-procedure
What are the main symptoms of urinary obstruction?
Pain - Flank with radiation to anterior and down to perineum or genital area
Severe, onset relatively acute, history of previous similar symptoms

Physical/lab - Flank tenderness, Hematuria
What are some intrinsic causes of urinary obstruction?
Blood clot
What are some extrinsic causes of urinary obstruction?
Crossing vessels
What are some radiographic signs of obstruction?
Delayed excretion of contrast
Dense nephrogram
Blunting of Forniceas - calyx
Dilatation of ureter, pelvis
Decreased or absent peristalsis in ureter
No contrast beyond point of obstruction
What us the UPJ?
Ureteropelvic junction
What are some characteristics of obstruction of the UPJ?
Most common congenital anomaly of the GU system in neonates
20% are bilateral
Intrinsic, 80% - defect in circular muscle
Extrinsic, 20% - crossing renal vessels
Treatment - pyeloplasty
What are some characteristics of renal calculi? Epidemiology?
5% of population, 20% at autopsy
50% recurrence of stone disease
Calcium oxalate, calcium phosphate, struvite calculi (magnesium ammonium phosphate - Infection stones)
Non-opaque - uric acid (gout, myeloproliferative disease)
Staghorn calculus
What are some radiographic features of renal calculi.
Most quickly and cheaply seen on KUB
Radiopaque calculus best on Non-contrast CT
Radiolucent best seen on IVP/non-contrast CT
Renal calculi can be seen on USN
What are the three most common locations of renal calculi?
UPJ - ureteropelvic junction
At crossing of pelvic vessels
UVJ - insertion of ureter into bladder
What are staghorn calculus?
They occupy nearly the entire collecting system
Association with Xanthogramulomatous Pylonephritis (XGP)
Increased chance of squamous cell cancer

Treatments include extra corporeal shock wave lithotripsy (ESWL), percutaneous removal (nephrostomy), open surgical stone removal or nephrectomy
What is a renal parenchymal tumor?
Renal cell adenocarcinoma - 80% of cases
Adenoma (early RCC) < 2 cm in size
Oncocytoma (epithelial cells of proximal tubule)
WIlms tumor - 5% (pediatrics)
What is a mesenchymal tumor?
Angiomyolipoma - contains fat, smooth muscle, and blood vessels - usually no calcifications
What are renal pelvis tumors?
Transitional cell tumors - 40-80% have associated bladder tumors
Squamous cell - associated with chronic irritation (XGN)
What are bladder/ureter tumors?
Transitional cell tumors
Squamous cell-chronic irritation
What are some characteristics of renal cell carcinomas?
Most frequent renal parenchymal tumor, origin from tubular epithelium
Spread locally to hilar lymph nodes
Spread to renal vein and then to IVC and to right atrium
Distal metastasis to lung, bone, brain, everywhere.
Very vascular - possible bleeding
What are some characteristics of uroepithelial tumors?
Transitional cell
Squamous cell - relationship to chronic irritation, infection, stone, XGN, pyelonephritis
Location - Calyces, Pelvis, Ureter, Bladder