Israel Medical Association Journal

Background: Acute focal nephritis is an inflammatory process of the renal parenchyma affecting principally the cortex of the kidney. It is considered a midpoint in the spectrum of upper urinary tract infections, ranging from uncomplicated pyelonephritis to intrarenal abscesses, and until recently the hyperechoic sonographic appearance of this lesion was considered uncommon.  

Objectives: To determine the relative prevalence of hyperechoic and hypoechoic sonographic appearance of focal renal lesions in patients with the clinical diagnosis of acute pyelonephritis and to correlate the findings with those of the color Doppler examinations.

Methods: We reviewed the sonograms of 367 patients hospitalized with the clinical diagnosis of acute pyelonephritis. The sonograms were reviewed for acute renal inflammatory changes. When a focal lesion was detected, we noted the echogenicity, side, form, location and color Doppler characteristics.

Results: Abnormal sonographic findings related to the infection were found in 78 cases. In 52 patients a focal lesion was diagnosed. Forty-seven focal lesions appeared hyperechoic related to the adjacent parenchyma. These lesions were more frequently located at the upper pole and were wedge-shaped in most of the cases. The areas appeared hypo/avascular on the color Doppler examination.

Conclusions: Our data suggest that the most common appearance of acute focal nephritis is an area of increased echogenicity in the parenchyma of the affected kidney.
 

Background: Familial nephritis is a heterogeneous group of disorders caused by several genetic conditions such as Alport syndrome, glomerulonephritic syndromes, and unclas­sified nephritis without deafness or ocular defects.

Objectives: To describe a family of Iraqi Jewish origin, several of whose members suffer from non-syndromic renal failure without deafness or ocular defects and where transmis­sion is by autosomal dominant inheritance. We present the case histories of four family members and describe the molecular analysis performed in order to seek a possible linkage to one of the genes causing Alport or Alport-like syndromes.

Methods: We investigated all family members over the age of 18 for evidence of renal failure. We also extracted DNA and carried out molecular linkage analysis with polymorphic markers in each of the known loci involved in Alport and Alport­like syndromes.

Results: Histology of the renal biopsy specimens showed non-specific findings. Linkage was excluded for all the Alport and Alport-like syndrome loci.

Conclusions: The condition suffered by several members of this family seems to represent a unique autosomal dominant type of progressive hereditary nephritis, characterized by hypertension and progressive renal failure without significant hematuria or proteinuria. The main histological changes are non-specific in the early stage of the disease. Our study rules out all the currently known genes that cause Alport syndrome as being responsible for the basic defect in this type of nephritis.