Doenças tubulo-intersticiais do rim

Question 1

Acute Interstitial

Nephritis

Answer 1

Acute interstitial nephritis (AIN) is a clinicopathologic
entity defined as a sudden decrease in renal function caused
by acute infiltration of inflammatory cells into the interstitial
compartment of the kidney (Web Figs. 30-1 and 30-2). AIN
accounts for up to 10% to 20% of all cases of acute kidney
injury (AKI).

Question 2

CLINICAL PRESENTATION

Answer 2

The typical presentation of AIN is a sudden decrease in renal
function in an otherwise asymptomatic patient recently
begun on a new medication. The classic clinical triad of
fever, rash, and eosinophilia are manifestations of a systemic
hypersensitivity reaction, and any or all of these may be seen
in AIN. Another fairly common symptom is lumbar or flank
pain, possibly due to distention of the renal capsule. It is
important to note that most patients do not have any of
these features, and their absence does not preclude the diagnosis
of AIN. Importantly, hypertension and edema, features
of acute glomerulonephritis, are uncommon in AIN.

Question 3

Characteristic laboratory tests include elevation of serum
creatinine, consistent with acute kidney injury, sterile pyuria,
and white blood cell casts. Hansel stain of the urine may
demonstrate eosinophils. Although eosinophiluria is strongly
suggestive of AIN, it is often not observed. Patients commonly
have non-nephrotic range proteinuria (<1 g per day)
and microscopic hematuria. Red blood cell casts are rarely
seen. Eosinophilia may be seen on the peripheral blood
smear.

Answer 3

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Question 4

ETIOLOGY

Answer 4

Drug reactions are the most common cause of AIN.
Antibiotics are the most common offenders, most notably
penicillins, cephalosporins, trimethoprim-sulfamethoxazole,
and ciprofloxacin. Nonsteroidal anti-inflammatory
drugs (NSAIDs) are a well-described cause of AIN, as are
proton pump inhibitors such as omeprazole. The second
most common cause of AIN is systemic infection. AIN may
also be associated with acute pyelonephritis and autoimmune
disease. A list of frequent causes of AIN is shown in
Table 30-1.

Question 5

TREATMENT AND PROGNOSIS

Answer 5

Treatment of AIN consists of removal of any suspected
offending drug or treatment of the underlying infection or
disorder. In cases in which antibiotics are being used to treat
infection, another appropriate drug should be substituted.
A short treatment with high-dose corticosteroids (prednisone,
1 mg/kg per day for a minimum of 2 weeks) may
accelerate recovery if used early in the clinical course.
Most cases of AIN resolve completely after the offending
factor has been removed. However, the longer the patient
remains in renal failure, the less likely it is that complete
recovery of renal function will occur.

Question 6

Chronic Interstitial

Nephritis

Answer 6

Chronic interstitial nephritis (CIN) is a clinicopathologic
entity defined as slowly progressive renal insufficiency due
to tubular cell atrophy and progressive interstitial fibrosis caused by a chronic interstitial mononuclear cell infiltrate
(Web Fig. 30-3). CIN is responsible for 15% to 30% of all
cases of end-stage renal disease (ESRD).

Question 7

CLINICAL PRESENTATION

Answer 7

Patients with CIN are usually asymptomatic until they
develop advanced chronic kidney disease (CKD), which is
characterized by symptoms of uremia: fatigue, malaise,
nausea, nocturia, and sleep disturbance. Patients, might,
however present earlier with features of the primary disease
that has caused the CIN (see “Etiology” below). CIN is
sometimes found incidentally on routine laboratory work
(Table 30-2).

Question 8

Laboratory studies reveal a glomerular filtration rate
(GFR) that falls over time, characterized by a slowly rising
serum creatinine. Urinalysis commonly reveals nonnephrotic
range proteinuria (<1 g per day) and may show
microscopic hematuria and pyuria. Because CIN is primarily
a disease of the tubules, specific findings of tubular dysfunction
might be out of proportion to the degree of renal
insufficiency. Examples include lead toxicity and multiple
myeloma, which primarily affect the proximal tubule and
may present as a proximal renal tubular acidosis (RTA),
glycosuria, aminoaciduria, and uricosuria. Chronic urinary
obstruction usually causes distal tubular damage and may
result in distal RTA, salt wasting, and hyperkalemia. Diseases
such as analgesic nephropathy, sickle cell disease, and
polycystic kidney disease affect the medullary collecting tubules and may cause polyuria due to urinary concentrating
defects.

Answer 8

ETIOLOGY
Many conditions are associated with CIN (Table 30-3). This
section highlights the more common causes and describes
the appropriate treatment and prognosis for each.

Question 9

Metabolic Disturbances

Answer 9

Analgesic Nephropathy

Question 10

Lead Nephropathy (chumbo)

Answer 10

Chinese Herb Nephropathy

Question 11

Sarcoidosiss

-hipercalcemia

Answer 11

Multiple Myeloma

Question 12

Urinary Tract Obstruction

Answer 12

Urinary tract obstruction is discussed in more detail elsewhere
in this chapter. Both acute urinary obstruction and
chronic urinary obstruction are associated with a mononuclear
cell interstitial infiltrate. Urinary obstruction causes
CIN accompanied by impaired excretion of hydrogen ions
and potassium and a vasopressin-resistant concentrating
defect.
Treatment is relief of the obstruction, which results in
halting the progression of loss of renal function.

Question 13

Radiation Nephritis

Answer 13

Hypertensive Arterionephrosclerosis

One of the most common causes of chronic kidney disease
in the United States, hypertensive arterionephrosclerosis,
begins with arteriolopathy in the afferent arterioles leading
to interstitial and glomerular changes likely related to
ischemia. Tubular atrophy and interstitial fibrosis are prominent
causes of the loss of renal function in these patients.
This topic is discussed in detail in Chapter 31.