Chronic IN

Analgesic nephropathy is the prototype

VESICOURETERAL REFLUX AND REFLUX NEPHROPATHY
Reflux nephropathy is the consequence of vesicoureteral reflux (VUR) or other urologic
anomalies in early childhood. It was previously called chronic pyelonephriti. Loss of
functioning nephrons leads to hypertrophy of the remnant glomeruli and eventual
secondary FSGS

SICKLE CELL NEPHROPATHY- type 4 RTA

Analgesic nephropathy -In its classic form, analgesicnephropathy is characterized by renal

insufficiency, papillary necrosis (Table 340-3) attributable to the presumed concentration of the
drug to toxic levels in the inner medulla, and a radiographic constellation of small, scarred
kidneys with papillary calcifications best appreciated by
computed tomography . a form of chronic interstitial nephritis.

Most patients have no symptoms referable to the urinary tract, although flank pain or hematuria
from a sloughed or obstructing papilla may occur. Some patients (more commonly women)
report a history of urinary tract infections
Hypertension is commonly seen with moderate to advanced disease. In studies cited above,
hypertension was present in up to 70 percent of patients

Other common problems include somatic complaints, such as malaise and weakness, and a
history of peptic ulcer disease that may be related, in part, to aspirinand/or nonsteroidal anti-
inflammatory drug (NSAID) ingestion

Laboratory manifestations — The major laboratory manifestations include an elevated serum

creatinine and a urinalysis showing hematuria or sterile pyuria. Patients usually have only mild
proteinuria (<1.5 g/day) [1,14]. Although more prominent proteinuria (≥3.5 g/day) may occur
among patients with advanced disease

Patients with classic radiographic findings — Among patients with classic radiographic findings,
the differential diagnosis includes all causes of papillary necrosis such as sickle cell disease,
chronic pyelonephritis, diabetes, and renal tuberculosis.

Patients who do not have classic radiographic features — Among patients who do not have
characteristic radiographic features, the differential diagnosis includes nephrosclerosis and other
forms of chronic interstitial nephritis such as sarcoidosis and infection-related acute interstitial
nephritis (including tuberculosis), aristolochic acid containing herb nephropathy, myeloma
kidney, medullary cystic kidney disease, medullary sponge kidney, and hypercalcemia

Li - Lithium accumulates in principal cells of the collecting duct by entering through the
epithelial sodium channel (ENaC), where it inhibits glycogen synthase kinase 3β and
downregulates vasopressin-regulated aquaporin water channels. Less frequently, chronic
tubulointerstitial nephritis develops after prolonged (>10–20 years) lithium use and is most likely
to occur in patients who have experienced repeated episodes of toxic lithium levels

CALCINEURIN-INHIBITOR NEPHROTOXICITY
The calcineurin inhibitor (CNI) immunosuppressive agents Cyclops

Early signs of chronic lead intoxication are attributable to proximal tubule

dysfunction, particularly hyperuricemia as a result of diminished urate secretion. The triad of
“saturnine gout,” hypertension, and renal insufficiency should prompt a
practitioner to ask specifically about lead expo

Differential diagnosis — from ATN- and glomerulonephritis--->granular and epithelial cell casts
and free epithelial cells in acute tubular necrosis; red cell casts, as well as red and white cells in
acute glomerulonephritis

Among patients with a predominance of white blood cells and white blood cell casts, renal
atheroemboli should be considered, particularly among older patients [66]. Similarly to AIN,
renal atheroemboli may present with eosinophiluria, eosinophilia, and skin lesions. However, the
skin lesions associated with atheroemboli are more commonly reticular (livedo reticularis) with
digital infarcts, whereas the characteristic rash associated with AIN is a diffuse, maculopapular
one

Among patients who have a completely negative sediment, obstruction should be considered as
part of the differential diagnosis