Nephritis is inflammation of the nephrons in the kidneys.

The word
"nephritis" was imported from Latin, which took it from Greek:
νεφρίτιδα.The word comes from the Greek νεφρός - nephro- meaning "of
the kidney" and -itis meaning "inflammation". Nephritis is often caused
by infections, toxins, and auto-immune diseases.

Nephritis is an older term used to clinically denote a child with

hypertension, decreased renal function, hematuria, and edema.
Technically, nephritis suggests a noninfectious inflammatory process that
involves the nephron; glomerulonephritis (GN) generally is a more
precise term.

1
 Incidence and prevalence of nephritis in the pediatric population is
unknown. Acute post infectious (most often post streptococcal) GN has
diminished in recent years but is still the most frequent. Other conditions
sometimes presenting with nephritis, such as membranous proliferative
GN, Alport syndrome, and SLE are infrequent.

Mortality/Morbidity

A child with nephritis might die of potential complications of severe

hypertension (eg, cerebral hemorrhage) or
complications of renal failure (eg,
hyperkalemia). Generally, fatal outcome is
rare. Children with post infectious GN usually
have complete recovery.
Children with chronic GN may develop morbidity secondary to hypertension,
chronic renal failure, complications of end-stage renal disease, or
complications of the primary disease (eg, SLE).
Over the last 3 decades, an important increase in the survival of children
with SLE has been observed, especially in those patients with renal
involvement. Management with immunosuppressive drugs (eg, intravenous
cyclophosphamide, azathioprine) has changed the prognosis in these
children. Children with SLE have increased life expectancy but are now
faced with new types of morbidity because of the squeal related to the
disease.
When nephritis leads to acute or chronic renal failure, associated morbidity
may occur. TIN is an unusual cause of death in children. The prognosis for
complete recovery of acute renal failure in TIN is excellent. The prognosis
for recovery with chronic TIN depends on the primary disease.

2
Race

Nephritis may occur in people of all races. The

race of the child is not generally helpful in
determining the primary etiology of GN. No racial
differences have been reported for the incidence
of nephritis in children.

Sex

Acute post streptococcal GN and IgA nephropathy occur more frequently in

males than in females. SLE is more frequent in females. TIN occurs with
equal frequency in both sexes.

Age

Acute post infectious GN usually occurs in

children older than 2 years. IgA nephropathy
is rare before adolescence.
Membranoproliferative GN tend to occur in
children older than 8 years. SLE can occur in
people of any age but is more frequent in
adolescents. Age is not usually very helpful in
determining the path biology of nephritis.
TIN is very rare in children younger than 5
years. Acute TIN can potentially occur in
people of any age. Chronic TIN tends to occur
late in childhood or adolescence with
obstructive uropathy or reflux. Chronic TIN
may occur in younger patients with inherited metabolic diseases.

3
SUBTYPES:
Nephritis syndrome can be described as a collection of various
signs and symptoms that are associated with those disorders that
affect the kidney, especially glomerular disorders. There are
different types of nephritis that people can suffer from. These the
common types of nephritis of the kidneys can affect people
include:

Glomerulonephritis is inflammation of the glomeruli. (When the term

"nephritis" is used without qualification, this is often the condition meant.)
Interstitial nephritis or tubulo-interstitial nephritis is inflammation of the
spaces
between
renal tubules.

Pyelonephritis is inflammation that results from a urinary tract infection that

reaches the pyelum (pelvis) of the kidney.
Lupus nephritis is an inflammation of the kidney caused by systemic
lupuserythematosus (SLE), a disease of the immune system.

4
 GLOMERULONEPHRITIS

Glomerulonephritis is inflammation of the glomeruli.

Causes

Glomerulonephritis may be caused by specific problems with the body's

immune system. Often, the precise cause of glomerulonephritis is unknown.
Damage to the glomeruli causes blood and protein to be lost in the urine.
The condition may develop quickly, with loss of kidney function occurring
over weeks and months (called rapidly progressive glomerulonephritis).
In about a quarter of people with chronic glomerulonephritis there is no
history of kidney disease and the disorder first appears as chronic renal
failure.

The following increase risk of developing this condition:

 History of cancer
 Blood or lymphatic system disorders
 Exposure to hydrocarbon solvents
 Infections such as strep infections, viruses, heart infections,or abscesses
 Diabetes
5
 Many conditions are known to cause or increase the risk for glomeru-
lonephritis, including:

 Focal segmental glomerulosclerosis

 Good pasture syndrome
 Membranoproliferative GN
 IgA nephropathy
 Lupus nephritis or Henoch-Schonlein
purpura
 Anti-glomerular basement membrane antibody disease
 Blood vessel diseases such as vasculitis or polyarteritis
 Amyloidosis

Non Proliferative

This is characterized by the numbers of cells (lack of hyper cellularity) in

the glomeruli. They usually cause nephrotic syndrome. This includes the
following types:

Minimal change GN

This form of GN causes 79.4% of nephrotic syndrome in children, but only

20% in adults. As the name indicates, there are no changes visible on
simple light microscopy, but on electron microscopy there is fusion of
podocytes (supportive cells in the glomerulus).
Immunohistochemistry staining is negative. Treatment consists of
supportive care for the massive fluid accumulation in the patient’s body (=
edema) and as well as steroids to halt the disease process (typically
Prednisone 1 mg/kg). Over 90% of children respond well to steroids, being
essentially cured after 3 months of treatment.
Adults have a lower response rate (80%). Failure to respond to steroids
('steroid resistant') or return of the disease when steroids are stopped
6
 ('steroid dependent') may require cytotoxic therapy (such as cyclosporin)
which is associated with many side-effects.

Focal Segmental Glomerulosclerosis (FSGS)

FSGS may be primary or secondary to

reflux nephropathy, Alport syndrome,
heroin abuse or HIV. FSGS presents as a
nephrotic syndrome with varying degrees of
impaired renal function (seen as a rising
serum creatinine, hypertension).
As the name suggests, only certain foci of
glomeruli within the kidney are affected,
and then only a segment of an individual glomerulus. The pathological
lesion is sclerosis (fibrosis) within the glomerulus and hyalinization of the
feeding arterioles, but no increase in the number of cells (hence non-
proliferative).
The hyaline is an amorphous material, pink, homogeneous, resulting from
combination of plasma proteins, increased mesangial matrix and collagen.
Staining for antibodies and complement is essentially negative.
Steroids are often tried but not shown to be effective. 50% of people with
FSGS continue to have progressive deterioration of kidney function, ending
in renal failure.

Membranous glomerulonephritis

Membranous glomerulonephritis (MGN), a relatively common type of

glomerulonephritis in adults, frequently produces a mixed nephrotic and
nephritic picture.
Its cause is usually unknown, but may be associated with cancers of the
lung and bowel, infection such as hepatitis and malaria, drugs including

7
 penicillamine, and connective tissue diseases such as systemic lupus
erythematosus.
Individuals with cerebral shunts are at risk of developing shunt nephritis,
which frequently produces MGN.
Microscopically, MGN is characterized by a thickened glomerular basement
membrane without a hypercellular glomerulus. Immunofluorescence
demonstrates diffuse granular uptake of IgG.
The basement membrane may completely surround the granular deposits,
forming a "spike and dome" pattern. Tubules also display the symptoms of
a typical Type III hypersensitivity reaction, which causes the endothelial
cells to proliferate, which can be seen under a light microscope with a PAS
stain.
Prognosis follows the rule of thirds: one-third remain with MGN indefinitely,
one-third remit, and one-third progress to end-stage renal failure. As the
glomerulonephritis progresses, the tubules of the kidney become infected,
leading to atrophy and hyalinisation. The kidney appears to shrink.
Treatment with corticosteroids is attempted if the disease progresses.
In extremely rare cases, the disease has been known to run in families,
usually passed down through the females. This condition, similarly, is called
Familial Membranous Glomerulonephritis. There have only been about nine
documented cases in the world.

Proliferative

This type is characterized by increased number of cells in the glomerulus

(hyper cellular). Usually present as a nephritic syndrome and usually progress
to end-stage renal failure (ESRF) over weeks to years (depending on type).

8
IgA nephropathy (Berger's disease)

IgA nephropathy is the most common type of glomerulonephritis in adults

worldwide. It usually presents as macroscopic haematuria (visibly bloody
urine).
It occasionally presents as a nephrotic syndrome. It often affects young
males within days (24-48hrs) after an upper respiratory tract or
gastrointestinal infection. Microscopic examination of biopsy specimens
shows increased number of mesangial cells with increased matrix (the
'cement' which holds everything together). Immuno-staining is positive for
immunoglobulin A deposits within the matrix. Prognosis is variable, 20%
progress to ESRF. ACE inhibitors are the mainstay of treatment.

Summary

This is a form of GN characterised by IgA deposits in the mesangeial regions

and immunocytochemistry is required for definitive diagnosis of the disease.

Presentation

1. Recurrent gross or microscopic hematuria

 gross hematuria occurs post-infection of the respiratory (more

common), gastrointestinal, or urinary tract

1. mild proteinuria
2. occasionally nephrotic syndrome (although it usually has a nephritic
presentation)
3. rarely, presents with crescent Rapidly progressive GN

9
Causes

The disease can be primary or secondary to liver and intestinal diseases. It

also overlaps with Henoch-Schonlein purpura, a systemic renal disease in
children in which similar IgA deposits occur.

Pathology

Plasma polymeric IgA is increased in IgA Nephropathy, and circulating IgA-

containing immune complexes can be found in the blood of some patients.
Plasma IgA is usually monomeric and polymeric plasma IgA is broken down in
the liver. IgA is normally found in mucus.

There are two forms of IgA and only IgA1 causes nephrogenicity.

Histology

Characteristic finding:

1. IgA deposition in the mesangium seen by immunofloresence

2. Electron dense deposits in electron microscopy
3. Absence of early complement components

May find:

1. normal glomeruli
2. mesangioproliferative GN
3. focal proliferative GN (healing may cause focal segmental sclerosis)
4. overt cresentic glomerulonephritis
5. leukocytes in glomerular capillaries

10
Post-infectious

Post-infectious glomerulonephritis can occur after essentially any infection,

but classically occurs after infection with Streptococcus pyogenes. It
typically occurs 10–14 days after a skin or pharyngeal infection with this
bacterium.
Patients present with signs and symptoms of glomerulonephritis. Diagnosis
is made based on these findings in an individual with a history of recent
streptococcal infection. Streptococcal titers in the blood (antistreptolysin O
titers) may support the diagnosis.
Light microscopy demonstrates diffuse endocapillary hypercellularity due to
proliferation of endothelial and mesangial cells, as well as an influx of
neutrophils and monocytes. The Bowman space is compressed, in some
cases to the extent that this produces a crescent formation characteristic of
crescentic glomerulonephritis.
Biopsy is seldom done as the disease usually regresses without
complications. Treatment is supportive, and the disease generally resolves
in 2–4 weeks.

Membranoproliferative/mesangiocapillary GN

Lop a 'tram-track' appearance, due to duplication and splitting. This may be

primary, or secondary to SLE, viral hepatitis, or hypocomplementemia. One
sees 'hypercellular and hyperlobular' glomeruli due to proliferation of both
cells and the matrix within the mesangium. Usually presents with a
combined nephritic-nephrotic picture, with inevitable progression to end
stage renal failure. The primary form consists of two types:
Type 1 (Classical and Alternative Complement activation)
Type 2 (also known as Dense Deposit Disease) Alternative Complement
activation only. C3 Nephritic Factor stabilizes C3 convertase, leading to
Hypocomplementemia. Unlike Type 1, no IgG is detected.
11
Rapidly progressive glomerulonephritis

Crescentic glomerulonephritis induced by infective endocarditis on PAS staining and

immunofluorescence. PAS staining (left) demonstrated circumferential and cellular
crescent formation with interstitial nephritis. Immunofluorescence (right)
demonstrated C3 positive staining in mesangial area.

Photomicrograph of renal biopsy showing crescent formation and tuft narrowing.

Periodic acid silver methenamine stain.

Rapidly progressive glomerulonephritis

(Crescentic GN) has a poor prognosis, with rapid progression to kidney failure over
weeks. Steroid therapy is sometimes used. Any of the above types of GN can be
rapidly progressive. Additionally two further causes present as solely RPGN.

One is Goodpasture's syndrome, an autoimmune disease whereby antibodies are

directed against basal membrane antigens found in the kidney and lungs. As well
as kidney failure, patient has hemoptysis (cough up blood). High dose

12
 immunosuppression is required (intravenous Methylprednisolone) and
cyclophosphamide, plus plasmapheresis. Immunohistochemistry staining of tissue
specimens shows linear IgG deposits.

The second cause is vasculitic disorders such as Wegener's granulomatosis and

polyarteritis. There is a lack of immune deposits on staining, but blood tests are
positive for ANCA antibody.

Histopathology: The majority of glomeruli present "crescents". Formation of

crescents is initiated by passage of fibrin into the Bowman space as a result of
increased permeability of glomerular basement membrane. Fibrin stimulates the
proliferation of parietal cells of Bowman capsule, and an influx of monocytes. Rapid
growing and fibrosis of crescents compresses the capillary loops and decreases the
Bowman space which leads to renal failure within weeks or months.

Symptoms

Common symptoms of glomerulonephritis are:

 Blood in the urine (dark, rust-colored, or brown urine)

 Foamy urine
 Swelling (edema) of the face, eyes, ankles, feet, legs, or abdomen

Symptoms that may also appear include the following:

 Abdominal pain
 Cough
 Diarrhea
 General ill feeling
 Fever
 Joint aches
 Muscle aches
 Loss of appetite
 Shortness of breath

13
Chronic renal failure symptoms may gradually develop.

Other symptoms that may occur with this disease:

 Excessive urination
 Nosebleed
 Blood in the vomit or in stools

Exams and Tests

Because symptoms develop gradually, the disorder may be discovered when

there is an abnormal urinalysis during a routine physical or examination for
unrelated disorders.
Glomerulonephritis can cause high blood pressure. It may only be
discovered as a cause of high blood pressure that is difficult to control.
Laboratory tests may reveal anemia or show signs of reduced kidney
functioning. A kidney biopsy confirms the diagnosis.
Later, signs of chronic kidney failure may be seen, including swelling
(edema), polyneuropathy, and signs of fluid overload, including abnormal
heart and lung sounds.
Imaging tests that may be done include:

 Abdominal CT scan
 Abdominal ultrasound
 Chest x-ray
 IVP

Urinalysis and other urine tests include:

 Examination of the urine under a microscope

 Creatinine clearance
 Total protein
 Uric acid, urine
 Urine concentration test
14
  Urine creatinine
 Urine protein
 Urine RBC
 Urine specific gravity

This disease may also affect the results of the following blood tests:

 Albumin
 Anti-glomerular basement membrane antibody test
 Anti-neutrophil cytoplasmic antibodies (ANCAs)
 BUN and creatinine
 Complement component 3
 Complement levels

Treatment

Treatment varies depending on the cause of the disorder, and the type and
severity of symptoms. High blood pressure may be difficult to control, and it
is generally the most important aspect of treatment.
Medicines that may be prescribed include:

 Blood pressure medications are often needed to control high blood pressure.
Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are
most commonly prescribed.
 Corticosteroids may relieve symptoms in some cases.
 Medications that suppress the immune system may also be prescribed,
depending on the cause of the condition.

A procedure called plasmapheresis may be used for some cases of

glomerulonephritis due to immune-related causes. The fluid part of the
blood containing antibodies is removed and replaced with intravenous fluids
or donated plasma (without antibodies). Removing antibodies may reduce
inflammation in the kidney tissues.

15
 Dietary restrictions on salt, fluids, protein, and other substances may be
recommended.
Persons with this condition should be closely watched for signs that they are
developing kidney failure. Dialysis or a kidney transplant may eventually be
necessary.

Outlook (Prognosis)

Glomerulonephritis may be a temporary and reversible condition, or it may

get worse. Progressive glomerulonephritis may lead to chronic kidney failure
and end-stage kidney disease.
If you have nephrotic syndrome and it can be controlled, other symptoms
may also be controlled. If it can't be controlled, end-stage kidney disease
may result.

Possible Complications

 Nephrotic syndrome
 Acute nephritic syndrome
 Chronic kidney failure
 End-stage kidney disease
 Hypertension
 Malignant hypertension
 Fluid overload -- congestive heart failure, pulmonary edema
 Chronic or recurrent urinary tract infection
 Increased susceptibility to other infections
 Hyperkalemia

Prevention

There is no specific way to prevent most cases of glomerulonephritis. Some

cases may be prevented by avoiding or limiting exposure to organic
solvents, mercury, and nonsteroidal anti-inflammatory drugs (NSAIDs).
16
 PYELONEPHRITIS

Pyelonephritis

macrophages and giant cells in a case of xanthogranulomatous pyelonephritis

Pyelonephritis (from the Greek πήληξ – pyelum, meaning "renal pelvis",

νεφρός – nephros, meaning "kidney", and -itis, meaning "inflammation") is
an ascending urinary tract infection that has reached the pyelum or pelvis
of the kidney.
It is a form of nephritis that is also referred to as pyelitis.
Severe cases of pyelonephritis can lead to pyonephrosis (pus accumulation
around the kidney), urosepsis (a systemic inflammatory response of the
body to infection), kidney failure and even death.
Pyelonephritis presents with fever, accelerated heart rate, painful urination,
abdominal pain radiating to the back, nausea, and tenderness at the
costovertebral angle on the affected side.
Pyelonephritis that has progressed to urosepsis may be accompanied by
signs of septic shock, including rapid breathing, decreased blood pressure,
violent shivering, and occasionally delirium.
Pyelonephritis requires antibiotic therapy, and sometimes surgical
intervention such as ureteroscopy, percutaneous nephrostomy or

17
 percutaneous nephrolithotomy, as well as treatment of any underlying
causes to prevent its recurrence.
Xanthogranulomatous pyelonephritis is a rare form of chronic pyelonephritis
in which nephrectomy (removal of the kidney) is usually necessary for
definitive treatment.

Epidemiology

The incidence of pyelonephritis is roughly 12–13 cases annually per 10,000

population in women receiving outpatient treatment and 3–4 requiring
admission.
In men, 2–3 per 10,000 are treated as outpatients and 1–2/10,000 require
admission. Young women are most often affected, probably reflecting
sexual activity in that age group.
Infants and the elderly are also at increased risk, reflecting anatomical
changes and hormonal status. Xanthogranulomatous pyelonephritis is most
common in middle-aged women.
It can present somewhat differently in children, in whom it may be
mistaken for Wilms' tumor.[22]

Causes

Most cases of "community-acquired" pyelonephritis are due to bowel

organisms that enter the urinary tract.
Common organisms are E. coli (70–80%) and Enterococcus faecalis.
Hospital-acquired infections may be due to coliform bacteria and
enterococci, as well as other organisms uncommon in the community (e.g.
Pseudomonas aeruginosa and various species of Klebsiella).
Most cases of pyelonephritis start off as lower urinary tract infections,
mainly cystitis and prostatitis.[1] E. coli can invade the superficial umbrella

18
 cells of the bladder to form intracellular bacterial communities (IBCs), which
can mature into biofilms.
These biofilm-producing E. coli are resistant to antibiotic therapy and
immune system responses, and present a possible explanation for recurrent
urinary tract infections, including pyelonephritis.[5] Risk is increased in the
following situations:[1][6]

 Mechanical: any structural abnormalities in the urinary tract,

vesicoureteral reflux (urine from the bladder flowing back into the
ureter), kidney stones, urinary tract catheterization, ureteral stents or
drainage procedures (e.g. nephrostomy), pregnancy, neurogenic bladder
(e.g. due to spinal cord damage, spina bifida or multiple sclerosis) and
prostate disease (e.g. benign prostatic hyperplasia) in men
 Constitutional: diabetes mellitus, immunocompromised states
 Behavioral: change in sexual partner within the last year, spermicide use
 Positive family history (close family members with frequent urinary tract
infections)

Signs and symptoms

Pyelonephritis can cause high fever,

pain on passing urine, and abdominal
pain that radiates along the flank
towards the back. There is often
associated vomiting.
Chronic pyelonephritis causes persistent
flank or abdominal pain, signs of
infection (fever, unintentional weight
loss, malaise, decreased appetite), lower urinary tract symptoms and blood
in the urine.

19
 Chronic pyelonephritis can in addition cause fever of unknown origin.
Furthermore, inflammation-related proteins can accumulate in organs and
cause the condition AA amyloidosis.
Physical examination may reveal fever and tenderness at the costovertebral
angle on the affected side

Diagnosis

Laboratory examination

Urinalysis may show signs of urinary tract infection. Specifically, the presence
of nitrite and white blood cells on a urine test strip in patients with typical
symptoms are sufficient for the diagnosis of pyelonephritis, and are an
indication for empirical treatment. Blood tests such as a complete blood count
may show neutrophilia. Microbiological culture of the urine, with or without
blood cultures and antibiotic sensitivity testing are useful for establishing a
formal diagnosis.[1]

Imaging studies

If a kidney stone is suspected (e.g. on the basis of characteristic colicky

pain or the presence of a disproportionate amount of blood in the urine), a
kidneys, ureters, and bladder x-ray (KUB film) may assist in identifying
radioopaque stones.[1] Where available, a noncontrast helical CT scan with
5 millimeter sections is the diagnostic modality of choice in the radiographic
evaluation of suspected nephrolithiasis.

All stones are detectable on CT scans except very rare stones composed of
certain drug residues in the urine.[10] In patients with recurrent ascending
urinary tract infections, it may be necessary to exclude an anatomical
abnormality, such as vesicoureteral reflux or polycystic kidney disease.

20
 Investigations used in this setting include ultrasonography of the kidneys or
voiding cystourethrography.[1] CT scan or abdominal ultrasonography is
useful in the diagnosis of xanthogranulomatous pyelonephritis; serial
imaging may be useful for differentiating this condition from kidney cancer.
[2]

Classification

Acute pyelonephritis

Acute pyelonephritis is an exudative purulent localized inflammation of the

renal pelvis (collecting system) and kidney.

The renal parenchyma presents in the interstitium abscesses (suppurative

necrosis), consisting in purulent exudate (pus): neutrophils, fibrin, cell debris
and central germ colonies (hematoxylinophils). Tubules are damaged by
exudate and may contain neutrophil casts. In the early stages, the glomerulus
and vessels are normal. Gross pathology often reveals pathognomonic
radiations of bleeding and suppuration through the renal pelvis to the renal
cortex.[citation needed]

Chronic pyelonephritis

Chronic pyelonephritis implies recurrent kidney infections, and can result in

scarring of the renal parenchyma and impaired function, especially in the
setting of obstruction. A perinephric abscess (infection around the kidney)
and/or pyonephrosis may develop in severe cases of pyelonephritis. [11]

Xanthogranulomatous pyelonephritis

Xanthogranulomatous pyelonephritis is an unusual form of chronic

pyelonephritis characterized by granulomatous abscess formation, severe
kidney destruction, and a clinical picture that may resemble renal cell

21
carcinoma and other inflammatory renal parenchymal diseases. Most patients
present with recurrent fevers and urosepsis, anemia, and a painful renal mass.
Other common manifestations include kidney stones and loss of function of the
affected kidney. Bacterial cultures of renal tissue are almost always positive. [12]
Microscopically, there are granulomas and lipid-laden macrophages (hence the
term xantho-, which means yellow in ancient Greek). It is found in roughly
20% of specimens from surgically managed cases of pyelonephritis. [2]

Management

In patients suspected of having pyelonephritis, a urine culture and antibiotic

sensitivity test is performed, and initial therapy is tailored on the basis of
the infecting organism. As most cases of pyelonephritis are due to bacterial
infections, antibiotics are the mainstay of treatment. The choice of antibiotic
depends on the species and antibiotic sensitivity profile of the infecting
organism, and may include fluoroquinolones, cephalosporins,
aminoglycosides, or trimethoprim/sulfamethoxazole, either alone or in
combination.[13]
In patients not requiring hospitalization where there is a low prevalence of
antibiotic-resistant bacteria, an oral fluoroquinolone such as ciprofloxacin or
levofloxacin is an appropriate initial choice for therapy. In areas where there
is a higher prevalence of fluoroquinolone resistance, it is useful to initiate
treatment with a single intravenous dose of a long-acting antibiotic such as
ceftriaxone or an aminoglycoside, and then continuing treatment with an
oral fluoroquinolone.
Oral trimethoprim/sulfamethoxazole is an appropriate choice for therapy if
the uropathogen is known to be susceptible. If
trimethoprim/sulfamethoxazole is used when the susceptibility is not
known, it is useful to initiate treatment with a single intravenous dose of a
long-acting antibiotic such as ceftriaxone or an aminoglycoside. Oral beta-

22
lactam antibiotics are less effective than other available agents for
treatment of pyelonephritis.[13]
People with acute pyelonephritis that is accompanied by high fever and
leukocytosis are typically admitted to the hospital for intravenous hydration
and intravenous antibiotic treatment. Treatment is typically initiated with an
intravenous fluoroquinolone, an aminoglycoside, an extended-spectrum
penicillin or cephalosporin, or a carbapenem. Combination antibiotic therapy
is often used in such situations. The treatment regimen is selected based on
local resistance data and the susceptibility profile of the specific infecting
organism(s).[13]
During the course of antibiotic treatment, serial white blood cell count and
temperature are closely monitored. Typically, the intravenous antibiotics are
continued until the patient is afebrile for at least 24 to 48 hours, then
equivalent oral antibiotic agents can be given for a total of 2–week duration
of treatment.[14] Intravenous fluids may be administered to compensate for
the reduced oral intake, insensible losses (due to the raised temperature)
and vasodilation and to optimize urine output. Percutaneous nephrostomy
or ureteral stent placement may be indicated to relieve obstruction caused
by a stone. Children with acute pyelonephritis can be treated effectively
with oral antibiotics (cefixime, ceftibuten and amoxycillin/clavulanic acid) or
with short courses (2 to 4 days) of intravenous therapy followed by oral
therapy. If intravenous therapy is chosen, single daily dosing with
aminoglycosides is safe and effective.[citation needed]
Treatment of xanthogranulomatous pyelonephritis involves antibiotics as
well as surgery. Nephrectomy is the best surgical treatment in the
overwhelming majority of cases, although polar resection (partial
nephrectomy) has been effective for some people with localized disease. [2]
[15]
Watchful waiting with serial imaging may be appropriate in rare
circumstances.[16]

23
Prevention

In people who experience recurrent urinary tract infections, additional

investigations may identify an underlying abnormality. Occasionally,
surgical intervention is necessary to reduce the likelihood of recurrence. If
no abnormality is identified, some studies suggest long-term preventive
(prophylactic) treatment with antibiotics, either daily or after sexual
activity.
In children at risk for recurrent urinary tract infections, meta-analysis of the
existing literature indicates that not enough studies have been performed to
conclude prescription of long-term antibiotics have a net positive benefit. [18]
Ingestion of cranberry juice has been studied as a prophylactic measure;
while studies are inconclusive, many suggest a benefit.[19][20] Increasing fluid
intake, consuming cranberry juice, blueberry juice, and fermented milk
products containing probiotic bacteria have all been shown to inhibit
adherence of bacteria to the epithelial cells of the urinary tract, and may
reduce the recurrence rate of urinary tract infections. [19]

INTERSTITIAL NEPHRITIS
Tubulointerstitial nephritis; Nephritis - interstitial; Acute interstitial (allergic)
nephritis

Interstitial nephritis is a kidney disorder in which the spaces between the

kidney tubules become swollen (inflamed). The inflammation can affect the
kidneys' function, including their ability to filter waste.

Causes, incidence, and risk factors

Interstitial nephritis may be temporary (acute) or it may be long-lasting (

chronic) and get worse over time.

24
The following can cause interstitial nephritis:

 Allergic reaction to a drug (acute interstitial allergic nephritis)

 Analgesic nephropathy

 Long-term use of medications such as acetaminophen (Tylenol),

aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDS). This is
called analgesic nephropathy

 Side effect of certain antibiotics (penicillin, ampicillin, methicillin,

sulfonamide medications, and others)

 Side effect of medications such as NSAIDs, furosemide, and thiazide

diuretics

The acute form of interstitial nephritis is common. It is most often caused by

side effects of certain drugs. This disorder may be more severe and more likely
to lead to chronic or permanent kidney damage in elderly people.

Symptoms

Interstitial nephritis can cause mild to severe kidney problems, including acute
kidney failure. In about half of cases, people will have decreased urine output
and other signs of acute kidney failure.

Symptoms of this condition may include:

 Blood in the urine

 Fever

 Increased or decreased urine output

 Mental status changes (drowsiness, confusion, coma)

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  Nausea, vomiting

 Rash

 Swelling of the body, any area

 Weight gain (from retaining fluid)

Signs and tests

An exam may show too much fluid under the skin or in the lungs (peripheral or
pulmonary edema). The health care provider might hear abnormal sounds
when listening to the heart or lungs with a stethoscope (auscultation). High
blood pressure is common.

Common tests include:

 Arterial blood gases

 Blood chemistry

 BUN and blood creatinine levels

 Complete blood count

 Kidney biopsy

 Urinalysis

 Urine osmolality

Treatment

Treatment focuses on the cause of the problem. Avoiding medications that lead
to this condition may relieve the symptoms quickly.

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Limiting salt and fluid in the diet can improve swelling and high blood pressure.
Limiting protein in the diet can help control the buildup of waste products in
the blood (azotemia) that can lead to symptoms of acute kidney failure.

If dialysis is necessary, it usually is required for only a short time.

Corticosteroids or anti-inflammatory medications can help in some cases.

Expectations (prognosis)

Most often, interstitial nephritis is a short-term disorder. In rare cases, it can

cause permanent damage, including chronic kidney failure.

Complications

Metabolic acidosis can occur because the kidneys aren't able to remove enough
acid. The disorder can lead to acute or chronic kidney failure or end-stage
kidney disease.

Prevention

In many cases, the disorder can't be prevented. Avoiding or reducing your use
of medications that can cause this condition can help reduce your risk.

LUPUS NEPHRITIS
Nephritis - lupus; Lupus glomerular disease

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Lupus nephritis is a kidney disorder that is a complication of systemic lupus
erythematosus.

Causes, incidence, and risk factors

Systemic lupus erythematosus (SLE, or lupus) is an autoimmune disease. This

means there is a problem with the body's immune system.

Normally, the immune system helps protect the body from harmful substances.
But in patients with an autoimmune disease, the immune system cannot tell
the difference between harmful substances and healthy ones. As a result, the
immune system attacks otherwise healthy cells and tissue.

SLE may damage different parts of the

kidney, leading to interstitial nephritis,
nephrotic syndrome, and membranous GN.
It may reapidly worsen to kidney failure.

Lupus nephritis affects approximately 3 out

of every 10,000 people. In children with SLE,
about half will have some form or degree of
kidney involvement.

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More than half of patients have not had other symptoms of SLE when they are
diagnosed with lupus nephritis.

SLE is most common in women ages 20 - 40. For more information, see:
systemic lupus erythematosus.

Symptoms

Symptoms of lupus nephritis include:

 Blood in the urine

 Foamy appearance to urine

 High blood pressure

 Swelling of any area of the body

For general lupus symptoms, see the article on SLE.

Signs and tests

A physical exam shows signs of decreased kidney

functioning with edema. Blood pressure may be
high. Abnormal sounds may be heard when the
doctor listens to the heart and lungs, indicating
fluid overload.

Tests that may be done include:

 ANA titer

 BUN and creatinine

 Lupus test

29
  Urinalysis

 Urine immunoglobulin light chain

A kidney biopsy is not used to diagnose lupus nephritis, but to determine what
treatment is appropriate.

This disease may also affect the results of the following tests:

 Complement component 3

 Complement

 Syphilis test

Treatment

The goal of treatment is to improve kidney function. Medicines may include

corticosteroids or other medications that suppress the immune system, such as
cyclophosphamide, mycophenolate mofetil, or azathioprine.

You may need dialysis to control symptoms of

kidney failure. A kidney transplant may be
recommended. (People with active lupus should
not have a transplant.)

Expectations (prognosis)

The outcome varies depending on the specific

form of lupus nephritis. Patients may have
acute flare-ups with alternating symptom-free
periods.

Some cases of lupus nephritis may progress to chronic kidney failure.

30
Although lupus nephritis may return in a transplanted kidney, it rarely leads to
end-stage kidney disease.

Complications

 Acute renal failure

 Chronic renal failure

 End-stage renal disease

 Nephrotic syndrome

Prevention

There is no known prevention for lupus nephritis.

Diet

In children with acute renal failure secondary to GN who have lost the ability to
excrete a water load, fluid restriction may prevent fluid overload.

TIN usually produces nonoliguric ARF. Fluid restriction of 300 mL/m 2/d plus
losses may allow management of acute renal failure for 2-3 days without
dialysis. In patients with hypertension, sodium restriction to recommended
daily allowances (RDA) of 2-4 mEq/kg/d may aid in management.

In children with renal failure, potassium restriction is justified to prevent

hyperkalemia. A short-term high-carbohydrate diet may prevent catabolism of
body protein as an energy source. Calcium supplementation is useful to
maintain normal serum calcium.
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Diet for Nephritis

Fasting on vegetable juices

The safest treatment for acute nephritis is fasting on vegetable juices for seven
to ten days. This will remove the toxins and systemic impurities responsible for
the inflammatory kidney conditions.

All-fruit diet

After the juice fast the patient may adopt an all-fruit diet for four or five days.
Thereafter, he may adopt a diet of fruits; and milk for about a week, and then
gradually adopt a well-balanced, low-protein vegetarian diet, with emphasis on
fresh fruits, and raw and steamed vegetables. In case of chronic nephritis, a
short juice fast for three days may be followed by a restricted diet for ten
days. Under this regimen, oranges or orange juice may be taken for breakfast.
Lunch may consist of salad made of raw vegetables in season, and dinner may
consist of one or two vegetables, steamed in their own juices, and a few nuts.

Well-balanced diet

Thereafter, the patient may gradually adopt a well-balanced, low-protein

vegetarian diet. Further juice fasts of short duration and a restricted diet for a
week should be undertaken at intervals of two or three months until such time
as the kidney condition shows signs of normalization.

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Avoid spinach and rhubarb, common salt

The patient should avoid vegetables containing large quantities of oxalic acid,
such as spinach and rhubarb. Chocolate and cocoa contain oxalic acid and
must not be taken. Common salt should be eliminated from the diet. Five or
six small meals should be taken in preference to a few large ones.

Activity

In patients with hypertension and renal failure, discourage strenuous activity;

however, walking, playing, and other activities are acceptable.

Further Inpatient Care

 Inpatient care is usually necessary only to manage severe hypertension

or complications of acute or chronic renal failure (eg, dialysis access,
uremic syndrome, congestive heart failure, electrolyte abnormalities such
as hyperkalemia and pericardial effusion). These problems are infrequent
in the general pediatric population.

Further Outpatient Care

 Outpatient care is an extension of inpatient care.

 Outpatient care may be as simple as observation in a child with
tubulointerstitial nephritis or resolving post streptococcal
glomerulonephritis (GN) or may involve antihypertensive, diuretics, and
diet modification as in a child with IgA nephropathy or
membranoproliferative GN and preserved renal function.
 Outpatient care may involve dialysis and transplantation in a child who
develops end-stage renal disease.

Inpatient & Outpatient Medications

33
  No specific change in medications is necessary for transition from
inpatient to outpatient care.

Transfer

 A physician who has experience in managing renal failure in children

should care for children with renal failure. In the United States, this is
frequently at a tertiary facility.

Complications

 Primary complications associated with hypertension

o Seizure
o Encephalopathy
o Stroke
o End-organ damage
 Primary complications associated with kidney failure
o Fluid overload
o Electrolyte abnormality
o Uremic symptoms
o Anemia
o Abnormal bone mineralization
o Sexual dysfunction
o Poor growth
o Anorexia
o Endocrine abnormalities

Patient Education

 Education about the specific nephritis is

helpful.

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  Encourage medication compliance and a healthy lifestyle (eg, ideal body
weight, no smoking, exercise, avoidance of risk behaviors).
 For excellent patient education resources, visit eMedicine's Kidneys and
Urinary System Center. Also, see eMedicine's patient education article
Blood in the Urine.

References

1. Nelson EG. Tubulointerstitial diseases. In: Goldman L, Ausiello D, eds. Cecil Medicine.
23rd ed. Philadelphia, Pa: Saunders Elsevier;2007:chap 123.
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Textbook of Rheumatology. 7th ed. St. Louis, Mo: WB Saunders; 2005.
a. Review Date: 8/12/2009.

b. Reviewed by: Parul Patel, MD, Private Practice specializing in Nephrology and
Kidney and Pancreas Transplantation, California Pacific Medical Center, San
Francisco, CA. Review provided by VeriMed Healthcare Network. Also reviewed
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3. URL of this page: http://www.nlm.nih.gov/medlineplus/ency/article/000484.htm

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