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ACUTE GLOMERULONEPHRITIS AND ITS CONSEQUENCES Category:   Articles ::  Health and Fitness  

ACUTE GLOMERULONEPHRITIS AND ITS CONSEQUENCES
Acute glornerulonephritis or nephritis is characterized by sudden onset of haematuria, oliguria, edema and hypertension. It is most common after 2 years of age, the age incidence being 2-12 years. Males are more frequently affected. It is one of the commonest causes of renal disease in kidney are inflamed.

The filtered material, which contains both waste products and substances vital for your health, passes into the tubules. From there, waste byproducts — urea, uric acid and creatinine — are excreted in your urine, while substances your body needs — sugar, amino acids, calcium and salts — are reabsorbed back into your bloodstream.


Etiology:

In all probability, it is secondary to a beta hemolytic Streptococcal infection of skin (serotype 49) or throat (serotype 12). A history of URTl, infected scabies or impetigo, 7 to 14 days previously is present in most cases. It is thought to be an immune mediated disease.

Causes of acute kidney failure are generally categorized in relation to where and how they affect your kidneys:

* Prerenal. These are problems that interfere with the flow of blood on its way to your kidneys.
* Renal. These are causes that result in direct damage to your kidneys.
* Postrenal. These are problems with the flow of urine after it leaves the kidneys on its way out of your body.

Pathologically, the kidney suffers as a result of deposition of soluble antigen-antibody complexes, resulting in proliferation and swelling of the endothelial cells. This leads to diminished blood flow through the kidney leading to fall in glomerular filtration.

It was previously shown variation in the copy number of gene FCGR3B is associated with susceptibility to a kidney disease called glomerulonephritis. In the new study, Timothy Aitman and colleagues determined variation in the number of FCGR3B copies is associated more broadly with autoimmune disorders, including lupus, microscopic polyangiitis, and Wegener's granulomatosis.

Clinical Features:

Signs of the disease are commonly revealed by presence of blood in the urine following an upper respiratory infection or cold, said Lifton. As the disease progresses, deposits of the immune-related antibody IgA, or immunoglobulin A, lead to scarring of the kidneys. Ultimately, a substantial fraction of patients develop kidney failure, and must rely on dialysis treatment or renal transplantation for survival.

A typical victim suffers from Streptococcal infection 1 to 2 weeks before, followed by acute onset of fever, puffiness of the face or mild leg (edema, malaise, headache, scanty micturition or passage of red or brown urine.

Examination reveals mild edema, most obvious in the face. There is elevation, to some extent, of blood pressure which may rarely cause hypertensive encephalopathy and convulsions.

Urinary findings:

a. Urine volume reduced
b. Specific gravity raised
c. Protein less than 2 gm /24 hours
d. Macroscopic or microscopic haematuria
e. RBC and granular casts

Other laboratory findings:

a. ASO titre and ESR are usually raised
b. Blood urea and creatinine moderately elevated
e. Serum electrolytes, especially potassium are raised .
f. Serum complement is low initially

Complications:

1. Acute renal failure
2. Acute left ventricular failure due to high blood pressure
3. Hypertensive encephalopathy

Differential Diagnosis :

1. Idiopathic nephrotic syndrome
2. Haemolylic uraemic syndrome
3. Anaphylactoid purpura
4. Acute pyelonephritis
5. IgA nephropathy
6. Hereditary nephritis

Diagnosis:

1. Clinical history of preceding Streptococcal infection
2. Passage of scanty, smoky or dirty brown urine
3. Laboratory investigations as above.

Treatment:

1. Rest in bed is essential in the acute phase, until the ESR returns to normal.

2. Accurate fluid balance charts are to be maintained. Daily weighing of the patient is also necessary.

3. In the acute phase, restrict fluid intake to 150-200 ml/M2/24 hours plus a volume equal to the urinary out put of the previous 24 hours.

4. In the absence of oliguria, hypertension, or edema, no active treatment other than penicillin is required.

5. Protein intake should be restricted to 20 gm/d.

6. Sodium and potassium intake should not exceed 25 mmol/d and 35 mmol/d respectively.

7. Penicillin should be prescribed at the start of treatment to eradicate haemolylic Streptococci.Oral penicillin V 250 mg qid and benzyl penicillin 500,000 units qid, both for 7-10 days.

8. The blood pressure and urine should he listed daily. If BP is mildly raised, phenobarbitone may be given twice daily at a dose of 30 mg.

9. Normal activities may be resumed when there is no evidence of over hydration, hypertension or cardiac failure and renal function is essentially normal.



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