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Renal Papillary Necrosis

 

·         Necrosis of the renal medullary pyramids and papillae with many causes, all of which mediate the development of ischemia

·         Infection is frequent finding, contributing to the clinical presentation of with fever and chills in about 2/3 of patients and positive urine cultures in 70%

o       But papillary necrosis can also develop without infection being present

·         Inflammatory reaction in the interstitium of the kidney compresses and compromises the medullary vasculature and predisposes the patient to ischemia and papillary necrosis

·         Other diseases can also impair this circulation, among them

o       Diabetes mellitus

o       Urinary obstruction

o       Analgesic nephropathy

§         Phenacetin, with its toxic metabolite, p-phenetidin

§         Also occurs with NSAIDS (non-steroidal anti-inflammatory drugs)

§         But usually with another predisposing factor present

·         Any condition associated with ischemia predisposes a person to papillary necrosis, such as

o       Shock

o       Dehydration

o       Hypovolemia

o       Sickle cell disease

o       Tuberculosis

o       Trauma

o       Cirrhosis = alcoholism

o       Coagulopathy

o       Renal vein thrombosis

o       Hemophilia

o       Christmas disease

o       Acute tubular necrosis

·         Most patients who develop papillary necrosis have two or more contributing factors

·         Usually bilateral

o       Can affect a single papilla or entire kidney may be involved

·         Mean age of onset is 53 years

o       More than 90% of cases occur in individuals older than 40

o       Uncommon in patients younger than 40 and in the pediatric population

·         More often in women than in men

·         Types

o       Focal = involves only the tip of the papilla

o       Diffuse = involves the whole papilla and parts of the medulla

o       Pathologically divided into medullary form and papillary form dictated by degree of ischemia

·         Clinical findings

o       Fever and chills

o       Flank and/or abdominal pain

o       Hematuria

o       Acute ureteral obstruction from sloughed papillae manifests as flank pain and colic from hydronephrosis or pyonephrosis

§         Hematuria is almost always present

§         Clinical picture in such cases may also include fever, chills and sepsis.

·         Imaging findings

o       The kidneys are usually normal in size until they contract in the late stages of the disease

o       Linear streak of contrast may appear inside of calyces representing void left by sloughed papilla (lobster claw sign)

o       Widening of the fornices from shrinking of the papillae

o       Larger collection of contrast may fill cavities inside of calyces representing a calyx without a papilla

o       Ring shadows can develop in the medulla outlining detached papilla within contrast material-filled cavity

§         Often in a triangular shape, referred to as the ring sign

o       Sloughed papillae can produce filling defects in internal collecting system or ureters

o       The ring shadow or sloughed papilla can rarely calcify

·         Complications

o       Infection

o       Obstruction

 

Coronal image of the left kidney  from a CT Urogram shows numerous irregular collections of contrast arising
from the calyces, some streak-like densities and overall distortion of the normal medullary-calyceal anatomy
For a larger version of this same photo, click here

 

References:   eMedicine  Jeffrey M Donohoe, MD, Pediatric Urology Fellow, Department of Urology, Vanderbilt University Medical Center. Jack H Mydlo, MD, Chief, Department of Urology, Woodhull Hospital; Chair and Professor, Department of Urology, Temple University School of Medicine.
Ali Nawaz Khan, MBBS, FRCP, FRCR, Consultant Radiologist, Department of Diagnostic Radiology, North Manchester General Hospital.
Muthusamy Chandramohan, MBBS, DMRD, FRCR, Special Registrar, Department of Radiology, Manchester Radiology
Sumaira Macdonald, MBChB, MRCP, FRCR, PhD, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute