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Updating the weights

Chapter 3 Artificial Neural Networks

3.3. Determining the weights

3.3.2 Updating the weights

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the studied patients. Hyperfiltration is injurious to the integrity of glomeruli; it leads to proteinuria and over time progress to glomerulosclerosis as seen in patients in this study. However, mesangio-proliferative glomerulonephritis may be difficult to explain in the absence of a primary glomerular nephritic process as in Berger’s disease.

Unfortunately, the study did not assay serum IgA or stain the kidney for IgA deposits.

However, benign haematuria was not observed in the patients.

Medullary lesions in sickle cell nephropathy consist of focal scarring and interstitial fibrosis with consequent tubular atrophy.53 Majority of the biopsied patients had significant interstitial fibrosis and tubular atrophy. This observation may further explain the prevalence of tubular dysfunction in this study. Although, papillary necrosis was not documented, the presence of interstitial nephritis as well as tubular dysfunction may not be unconnected with chronic analgesic use during episodes of painful crisis. Analgesic nephropathy therefore may have contributed to the magnitude of chronic kidney disease in the studied SCD patients.

CHAPTER SIX

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This study has highlighted the prevalence and pattern of chronic kidney disease among SCD patients in Ile-Ife. Chronic kidney disease is a common and prevalent complication of SCD.

Chronic kidney disease was characterized by a preponderance of tubular dysfunction and was severe in HbSS compared to HbSC. Chronic kidney disease was commoner in Hb-SS than Hb-SC patients.

Marked tubular dysfunction even in the presence of normal GFR suggests greater susceptibility of the tubule/interstitium to renal damage in sickle cell disease.

The common histological lesions documented in the biopsied patients were mesangioproliferative glomerulonephritis, minimal change disease, and focal segmental glomerulosclerosis. Majority of the patients had significant interstitial fibrosis and tubular atrophy which could have contributed to the magnitude of tubular dysfunction seen.

RECOMMENDATIONS AND LIMITATIONS RECOMMENDATIONS

95

Based on the observation of this study the following recommendations are hereby suggested:

1. Assessment of glomerular and tubular functions should be performed periodically in stable adult SCD patients.

2. Patients with glomerular or tubular dysfunction even with normal GFR should be managed by joint Nephrology/Haematology teams.

3. Large cohort studies on both adults and children with SCD will help to identify genetic and/or environmental risk factors that predispose patients to complications such as sickle cell renal disease. This will allow identification of susceptible individuals before the onset of established disease, address any modifiable risk factors and refer them to nephrology services in a timely fashion.

LIMITATIONS

1. Non-availability of facilities for immunofluorescence/immuno-peroxidase and electron microscopy.

2. β2-microglobulin should have been a better endogenous marker of tubular dysfunction.

3. Refusal of renal biopsy by a few of the subjects with CKD.

4. Inability to asses for proteinuria twice three months apart.

5. Use of estimated GFR instead of measured GFR in a muscle wasting chronic disease like SCD.

6. Use of urinalysis to screen for urinary tract infection.

96

7. Use of analgesics should have been documented because analgesic nephropathy could cause chronic interstitial nephritis and ultimately tubular dysfunction.

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