di 16.26
Reference:
Harding, Godfrey K.M., Zhanel, George G., Nicolle, Lindsay E., Cheang, Mary, the Manitoba
Diabetes Urinary Tract Infection Study Group, Antimicrobial Treatment in Diabetic Women with
Asymptomatic Bacteriuria. New England Journal of Medicine 2002 347: 1576-1583
Diposkan oleh Anti-Remed with MECO MMSA Tidak ada komentar:
Kirimkan Ini lewat EmailBlogThis!Berbagi ke TwitterBerbagi ke Facebook
scenario 5
di 07.44
Nb:nah ada beberapa diagnosis yang berkaitan dengan faktor penyebabnya diabetes..
-Pyelonephritis acute
Definition: Infection of the kidney.
Overview:
More common in women than in men.
Infection of the kidney can occur due to organisms spreading to the kidney from the bladder
(ascending infection) or from the bloodstream.
Ascending infection is more common.
E. Coli is the most common organism.
Abnormalities of the heart valves can be the source of organisms being spread by the bloodstream.
Types:
Bacterial
Fungal
Symptoms:
Typically the patient experiences flank pain (pain in the back just below the ribcage), fevers and
often nausea and vomiting.
The pain can be located in the upper right abdomen as well.
Kidney infection may or may not be accompanied by symptoms of bladder infection (see acute
cystitis) and on occasion the urine will have blood that is visible.
Complications:
If not treated completely and in a timely manner an abscess can form in the kidney or in rare cases
the infection can get into the bloodstream and make one very ill requiring hospitalization.
If pyelonephritis develops as a patient is passing a kidney stone, immediate intervention may be
necessary to decompress the kidney and allow proper drainage of the kidney for infection to clear.
Clinical Findings/signs:
Pyelonephritis remains a clinical diagnosis. The findings on examination include flank or upper
abdominal tenderness, fever and usually a positive urine analysis and culture for bacteria. Nausea and
vomiting are often present. If the bladder is infected there may be tenderness of the lower abdomen
overlying the bladder as well. Imaging with ultrasound, CT or other modality can be used when there
is suspicion of a stone or other complicating factor. Patients can have a wide range of symptoms
including septic physiology (critically low blood pressure and unstable vital signs) if the infection
has spread to the bloodstream.
Treatment:
Lifestyle there are no lifestyle modifications to decrease the chances of pyelonephritis unless one
is prone to recurrent bladder infections.
Medication Antibiotics are generally used to treat the infection. The length of time the patient is
on antibiotics depends upon the specific antibiotic and the clinical situation. Though most
pyelonephritis episodes can be treated on an outpatient basis, admission to the hospital may be
warranted for IV antibiotics.
Surgery: Surgical intervention may be necessary if the pyelonephritis is complicated by renal
abscess or a urinary stone. The type of surgery or intervention depends upon the clinical situation.
Occasionally the intervention can be performed by the radiologist without going under an anesthetic.
Prognosis: The prognosis for acute bacterial pyelonephritis is good assuming that there is no
complicating factor such as abcess, sepsis or stone. In children, whose kidneys are still developing,
bacterial pyelonephritis can cause scarring of the kidney tissue and, if recurrent, can lead to overall
decreased kidney function later in life.
-sindrom nefrotik
Nephrotic syndrome is a clinical picture of glomerular disease characterized by massive proteinuria>
3.5 gram/24 hours / 1.73 m 2 with hypoalbuminemia, edema anasarka, hyperlipidemia, lipiduria, and
hiperkoaguabilitas. Nephrotic syndrome can be caused by glomerulonephritis (GN) due to primary
and secondary infection, malignancy, drugs or toxins, connective tissue disease, systemic disease.
Abnormalities histopathological lesions in the SN SN includes a minimum of (MCNS), focal
segmental glomerulosclerosis (FSGS), mesangial proliferative glomerulonephritis (MPGN),
Membranoproliferative glomerulonephritis (MPGN), membranous glomerulopati
(GM). Management of nephrotic syndrome consists of specific and non specific treatment. Specific
treatment is aimed at the underlying disease, while non spseifik treatment aimed at reducing
proteinuria, edema, and treat complications. In patients with nephrotic syndrome accompanied by
diabetes, the use of corticosteroids administered with caution because it can increase blood sugar
levels. It has been reported the case of a man aged 59 years with swelling in both legs which when
pressed will form a basin, and it takes time to get back to normal. Painful urination and Anyang-
anyangan. Patient had a history of hypertension and diabetes mellitus. blood pressure 155/90 mmHg
Conjunctiva anemis epigastric tenderness and suprapubic region on both the inferior extremity edema
with pitting edema. decrease in hemoglobin levels (9.8 mg / dl), erythrocyte (3.59 million / mL), and
hematocrit (27.5%). Blood chemistry examination results when blood glucose increased (GDS 557 g
/ dl), decreased total protein (4.5), albumin (2.06), and globulin (2.43). Routine urine examination
results proteinuria (+3). Routine stool examination found the worm eggs. Abdominal ultrasound
examination within normal limits. patients diagnosed as nephrotic syndrome with diabetes mellitus
and UTI. Patients were given diuretic therapy, ACE inhibitors, and sliding scale insulin.
Keywords: Management; nephrotic syndrome; Diabetes mellitus
Therapy
Do restrictions on fluid intake with intravenous administration flabot/24 RL 1 hour and urinary
catheters. To reduce edema, furosemide administered once daily in the morning. To lower blood
pressure and proteinuria control, given captopril 6.25 mg orally three times daily. To control
hyperglycemia, given regular insulin sliding scale starting from 10 iu the sub cutaneous. Given
pirantel pamoate 500mg once a day to cope with worm infestation. For urinary tract infections,
ciprofloxacin 500 mg given twice daily.
Discussion
Nephrotic syndrome (SN) is a syndrome caused by various diseases that attack the kidneys and cause
edema, proteinuria 3.5 g/24 hours / 1.73 m2 or more than 3 + proteinuria by dipstick (or the ratio of
protein: creatinine more than 200 mg / mmol or> 2.0 mg / dL), decrease in blood levels of albumin
<3.5 g / dl (hipoalbiminemia), and increased levels of fats in the blood of more than 220 mg / dL
(hyperlipidemia), lipiduria, and hiperkoaguabilitas.
Nephrotic syndrome can be caused by glomerulonephritis (GN) of primary and secondary. Primary
GN is the commonest cause histologic abnormalities consisting of minimal SN lesions (MCNS),
focal segmental glomerulosclerosis (FSGS), mesangial proliferative glomerulonephritis (MPGN),
Membranoproliferative glomerulonephritis (MPGN), membranous glomerulopati (GM). Secondary
GN can be caused by infections (HIV, tuberculosis, leprosy, syphilis, malaria, skistosoma, hepatitis
virus B and C), malignancy, connective tissue diseases (SLE, rheumatoid arthritis), drugs or toxins
(NSAIDs, captopril, penisilinamin, heroin) , and the result of systemic disease (diabetes mellitus,
amyloidosis, preeclampsia, vesicoureteric reflux, etc.).
Treatment of nephrotic syndrome (SN) consists of specific treatments aimed at the basis of disease
and non-specific treatment to reduce proteinuria, edema control, and treat complications.
Diuretics with low-salt diet and bed rest may help control edema. In patients with oliguria
experiencing overload, diuretics may induce diuresis and urine output to stabilize again. The most
commonly used diuretics are loop diuretics, especially furosemide. Oral furosemide may be given
and if the resistance can be combined with a thiazide, metazolon, and or asetazolamid. In SN, there
can be resistant to furosemide. Some strategies to overcome the tubular resistance to furosemide in
SN include increasing doses of furosemide, a combination of furosemide and albumin, or in
combination with the diuretic furosemide acting on the distal tubule. The addition of 2-3 times the
dose of furosemide may overcome the decrease in proximal tubule transport.
ISKDC recommend starting steroid therapy with prednisone 60 mg / m 2 / day (or 2 mg / kg / day,
maximum 80 mg / day) in divided doses for 4 weeks. Dose was lowered to 40 mg / m 2 / day (or
1.5 mg / kg / day, maximum 60 mg / day) for 4 weeks. But the Arbeitsgemeinschaft fur Padiatrische
Nephrologie recommend giving steroids to alternate-day system for 4 weeks is more effective than
the way ISKDC. Failure to achieve remission after the administration of this therapy is called a state
of steroid resistance.
Control can improve proteinuria and hypoalbuminemia reduces the risk of complications. Restriction
of protein intake from 0.8 to 1.0 g / kg / day can reduce proteinuria. Angiotensin converting enzyme
inhibitors (ACE inhibitors) and angiotensin II receptor antagonists can reduce blood pressure and a
combination of both has an additive effect in reducing proteinuria. ACE inhibitors reduce proteinuria
by reducing intraglomerular capillary pressure by dilating the efferent arterioles and affect
glomerular permeability. Low dose of captopril or enalapril, and the dose increased after 2
weeks. Angiotensin converting enzyme inhibitors reduce glomerular protein ultrafiltration by
lowering pressure and fixing intrakapiler glomerular size selective glomerular barrier effect of this
drug antiproteinurik last long (about 2 months after the drug is stopped) Angiotensin receptor blocker
(ARB) were also able to improve proteinuri for inhibiting inflammation and fibrosis interstisium,
inhibiting the release of cytokines, growth factors, adhesion molecules due to the work of local
angiotensin II in the kidney.
Alkilating drugs, cyclophosphamide and chlorambucil are used in the treatment of steroid-
dependentSN and SRNS. Cyclophosphamide given remission longer than corticosteroids (75% for 2
years) at a dose of 2-3 mg / kg bw. / Day for 8 weeks. Side effects of cyclophosphamide is bone
marrow depression, infections, alopecia, hemorrhagic cystitis and infertility when administered over
6 months. Chlorambucil given at a dose of 0.1 to 0.2 mg / kg / day for 8 weeks. Chlorambucil side
effects were azoospermia and agranulocytosis. Because the cause of FSGS and MCNS-mediated
immune process, cyclosporine is an appropriate therapy for SRNS. Cyclosporine causes
immunosuppression especially T lymphocytes by inhibiting the production of interleukin-2 and other
lymphokines. Cyclosporine A may also be used in combination with prednisolone in the case of SN
in combination with other therapies fail. Drug side effects are gingival hyperplasia, hypertrichosis,
hiperurisemi, hypertension and nefrotoksis.
Non-steroidal anti-inflammatory drugs (NSAIDs), such as indomethacin 3x50mg. NSAIDs can be
used in patients with membranous nephropathy and focal segmental glomerulosclerosis to reduce
prostaglandins. This leads to renal vasoconstriction, decreased glomerular capillary pressure,
filtration surface area and reduces proteinuria to 75%. In addition NSAIDs may reduce fibrinogen
levels, and prevents platelet aggregation. However, to be concerned that NSAIDs cause a progressive
decline in renal function in some patients. This drug should not be given if the creatinine clearance
<50 ml / min.
Can be used to overcome the obstacle hidroxymethyl hiperlipidemi glutaryl co-enzyme A (HMG Co-
A) reductase is effective in lowering plasma cholesterol. Gemfibrozil, bezafibrat, klofibrat
significantly lowered triglyceride levels and slightly lower cholesterol levels. Klofibrat can be toxic
to normal levels due to increased levels of free klofibrat cause muscle damage and acute renal
failure. Probukol lower total cholesterol and LDL cholesterol, but minimal effect on
triglycerides. Nicotinic acid (niacin) can lower cholesterol and more effective when combined with
gemfibrozil. Cholestyramine and kolestipol effectively lower total cholesterol and LDL cholesterol,
but the drug is not recommended because of its effect on intestinal absorption of vitamin D in
vitamin D deficiency is exacerbated in the SN.
SN increased risk of thromboembolism and should receive treatment. Although the provision of long
term anticoagulation remains controversial but in one study proved beneficial. Fat-lowering drugs
known as statins, like simvastatin, pravastatin, and lovastatin can lower LDL cholesterol,
triglycerides, and increase HDL cholesterol.
In this case, patients suffering from nephrotic syndrome characterized by limb edema,
hypoalbuminemia (<3.5 g / dl) and proteinuria ( 3.5 g / day). Risk factors that are owned by the
patient and is likely to be the cause of the nephrotic syndrome is diabetes mellitus. The exact cause of
nephrotic syndrome can be detected by doing a kidney biopsy. In these patients required restriction
of fluid intake and restriction of protein intake for reducing proteinuria. Diuretic furosemide
administered orally to reduce edema. Also given the ACE inhibitor captopril has the effect of
lowering blood pressure and reduce proteinuria. In patients not given corticosteroid therapy.
Corticosteroids increase the occurrence of gluconeogenesis, the formation of glucose from protein, so
the risk of increasing blood sugar levels. In patients with diabetes mellitus, treatment with
corticosteroids SN there is need for caution in the administration. To work around this, if you do
have to take corticosteroids, the patient is expected to reduce consumption of sugar and
carbohydrates. Will have an effect is not good, especially on the use of corticosteroids in the long
term and high doses. In the patients were also given a sliding scale insulin for hyperglycemia.
Conclusion
Nephrotic syndrome is a clinical picture of glomerular disease characterized by massive proteinuria>
3.5 gram/24 hours / 1.73 m 2 with hypoalbuminemia, edema anasarka, hyperlipidemia, lipiduria, and
hiperkoaguabilitas. Nephrotic syndrome secondary to systemic disease may be caused by diabetes
mellitus. Management of nephrotic syndrome consists of specific and non specific treatment which
includes the control of edema (mainly with diuretics furosemide and bed rest), control of proteinuria
(by administering an ACE inhibitor, restriction of protein intake), corticosteroids, alkilating drugs,
NSAIDs, cyclosporine A, or therapies hyperlipidemia. In patients with diabetes mellitus, treatment
with corticosteroids SN need for prudence in the administration because the risk of increasing blood
sugar levels.
atau...
Antinuclear antibody
Cryoglobulins
Complement levels
Glucose tolerance test
Hepatitis B and C antibodies
HIV test
Rheumatoid factor
Serum protein electrophoresis (SPEP)
Syphilis serology
Urine protein electrophoresis (UPEP)
This disease may also change the results of the following tests:
Vitamin D level
Serum iron
Urinary casts
TREATMENT
The goals of treatment are to relieve symptoms, prevent complications, and delay kidney damage. To
control nephrotic syndrome, you must treat the disorder that is causing it. You may need treatment
for life.
Treatments:
Keep blood pressure at or below 130/80 mmHg to delay kidney damage. Angiotensin-
converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are the medicines most
often used. ACE inhibitors may also help decrease the amount of protein lost in the urine.
You may take corticosteroids and other drugs that suppress or quiet the immune system.
Treat high cholesterol to reduce the risk of heart and blood vessel problems. A low-fat, low-
cholesterol diet is usually not very helpful for people with nephrotic syndrome. Medications to reduce
cholesterol and triglycerides (usually statins) may be needed.
A low-salt diet may help with swelling in the hands and legs. Water pills (diuretics) may also
help with this problem.
Low-protein diets may be helpful. Your health care provider may suggest eating a moderate-
protein diet (1 gram of protein per kilogram of body weight per day).
You may need vitamin D supplements if nephrotic syndrome is long-term and not responding
to treatment.
Blood thinners may be needed to treat or prevent blood clots.
Definition
Nephrotic syndrome is a collection of symptoms which occur because the tiny blood vessels (the
glomeruli) in the kidney become leaky. This allows protein (normally never passed out in the
urine) to leave the body in large amounts.
Description
The glomeruli (a single one is called a glomerulus) are tiny tufts of capillaries (the smallest type
of blood vessels). Glomeruli are located in the kidneys, where they allow a certain amount of
water and waste products to leave the blood, ultimately to be passed out of the body in the form
of urine. Normally, proteins are unable to pass through the glomerular filter. Nephrotic
syndrome, however, occurs when this filter becomes defective, allowing large quantities of
protein to leave the blood circulation, and pass out or the body in the urine.
Patients with nephrotic syndrome are from all age groups, although in children there is an
increased risk of the disorder between the ages of 18 months and four years. In children, boys are
more frequently affected; in adults, the ratio of men to women is closer to equal.
Causes and symptoms
Nephrotic syndrome can be caused by a number of different diseases. The common mechanism
which seems to cause damage involves the immune system. For some reason, the immune
system seems to become directed against the person's own kidney. The glomeruli become
increasingly leaky as various substances from the immune system are deposited within the
kidney.
A number of different kidney disorders are associated with nephrotic syndrome, including:
minimal change disease or MCD (responsible for about 80% of nephrotic syndrome in children,
and about 20% in adults) MCD is a disorder of the glomeruli
focal glomerulosclerosis
membranous glomerulopathy
membranoproliferative glomerulonephropathy
Other types of diseases can also result in nephrotic syndrome. These include diabetes, sickle-cell
anemia, amyloidosis, systemic lupus erythematosus, sarcoidosis, leukemia, lymphoma, cancer of
the breast, colon, and stomach, reactions to drugs (including nonsteroidal anti-inflammatory
drugs, lithium, and street heroine), allergic reactions (to insect stings, snake venom, and poison
ivy), infections (malaria, various bacteria, hepatitis B, herpes zoster, and the virus which causes
AIDS), and severe high blood pressure.
The first symptom of nephrotic syndrome is often foamy urine. As the syndrome progresses,
swelling (edema) is noticed in the eyelids, hands, feet, knees, scrotum, and abdomen. The patient
feels increasingly weak and fatigued. Appetite is greatly decreased. Over time, the loss of protein
causes the muscles to become weak and small (called muscle wasting). The patient may note
abdominal pain and difficulty breathing. Because the kidneys are involved in blood pressure
regulation, abnormally low or abnormally high blood pressure may develop.
Over time, the protein loss occurring in nephrotic syndrome will result in a generally
malnourished state. Hair and nails become brittle, and growth is stunted. Bone becomes weak,
and the body begins to lose other important nutrients (sugar, potassium, calcium). Infection is a
serious and frequent complication, as are disorders of blood clotting. Acute kidney failure may
develop.
Diagnosis
Diagnosis is based first on the laboratory examination of the urine and the blood. While the urine
will reveal significant quantities of protein, the blood will reveal abnormally low amounts of
circulating proteins. Blood tests will also reveal a high level of cholesterol. In order to diagnose
one of the kidney disorders which cause nephrotic syndrome, a small sample of the kidney
(biopsy) will need to be removed for examination. This biopsy can be done with a long, very thin
needle which is inserted through the skin under the ribs.
Treatment
Treatment depends on the underlying disorder which has caused nephrotic syndrome.
Medications which dampen down the immune system are a mainstay of treatment. The first
choice is usually a steroid drug (such as prednisone). Some conditions may require even more
potent medications, such as cyclophosphamide or cyclosporine. Treating the underlying
conditions (lymphoma, cancers, heroine use, infections) which have led to nephrotic syndrome
will often improve the symptoms of nephrotic syndrome as well. Some patients will require the
use of specific medications to control high blood pressure. Occasionally, the quantity of fluid a
patient is allowed to drink is restricted. Some patients benefit from the use of diuretics(which
allow the kidney to produce more urine) to decrease swelling.
Key terms
Glomeruli Tiny tufts of capillaries which carry blood within the kidneys. The blood is filtered
by the glomeruli. The blood then continues through the circulatory system, but a certain amount
of fluid and specific waste products are filtered out of the blood, to be removed from the body in
the form of urine.
Immune system The complex system within the body which serves to fight off harmful
invaders, such as bacteria, viruses, fungi.
Kidney failure The inability of the kidney to excrete toxic substances from the body.
Prognosis
Prognosis depends on the underlying disorder. Minimal change disease has the best prognosis of
all the kidney disorders, with 90% of all patients responding to treatment. Other types of kidney
diseases have less favorable outcomes, with high rates of progression to kidney failure. When
nephrotic syndrome is caused by another, treatable disorder (infection, allergic or drug reaction),
the prognosis is very good.
REFERENCES
Appel GB. Glomerular disorders and nephrotic syndromes. In: Goldman L, Ausiello D, eds. Cecil
Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 122.
Nachman PH, Jennette JC, Falk RJ. Primary glomerular disease. In: Brenner BM, ed. Brenner and
Rector's the Kidney. 8th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 30.