Renal papillary necrosis
Renal papillary necrosis
Description, Causes and Risk Factors:
Necrosis of renal papillae, occurring in acute pyelonephritis, especially in diabetics, or in analgesic nephropathy; renal failure may result.
Renal papillary necrosis can be defined as a disorder of the renals (kidneys) involving death of some or all of the renal papillae. Renal papillary necrosis is also known as a renal medullary necrosis, Necrosis - renal papillae.
Renal papillary necrosis is the consequence of an ischemic process in the renal papillae. Infection that causes inflammation of the interstitium also may lead to compression of the medullary vasculature and thus predispose the vessels to ischemic change. Perfusion compromise as a consequence of vasculitis in diabetes mellitus, tuberculosis, or the curtailment of flow observed in hemoglobinopathy, analgesic nephropathy, or acute urinary obstruction, also sets the stage for ischemic changes in the medullary pyramid.
A useful mnemonic device for the conditions associated with renal papillary necrosis is POSTCARDS, which stands for the following:
Obstruction of the urinary tract.
Sickle cell hemoglobinopathies, including sickle cell trait.
Cirrhosis of the liver, chronic alcoholism.
Renal transplant rejection, radiation.
More than half the patients with renal papillary necrosis have 2 or more of these causative factors. Thus, renal papillary necrosis in most patients is multifactorial in origin, and physicians must consider the pathogenesis of renal papillary necrosis a combination of detrimental factors that overlap and operate in concert to cause renal papillary necrosis.
In the advanced stage of necrosis, clefts originate from the fornices and extend into and dissect the medullary pyramids and papillae, ultimately causing the papillae to slough. Caliceal deformities in renal papillary necrosis occur in three forms: medullary, papillary, and in situ.
Renal papillary necrosis generally affects individuals who are in the middle decades of life or older. The typical patient is aged 53 years, with nearly half of cases occurring in individuals older than 60 years and more than 90% of cases occurring in individuals older than 40 years. Renal papillary necrosis is uncommon in individuals younger than 40 years and in the pediatric population, except in patients with sickle cell hemoglobinopathies, hypoxia, dehydration, and septicemia.
In general, renal papillary necrosis is more common in women than in men. Mandel organized the first comprehensive review to focus attention on renal papillary necrosis.
Necrosis (tissue death) of the renal papillae may make the kidney unable to concentrate the urine. Symptoms may include:
Dark, rust-colored, or brown urine.
Tissue in the urine.
Back pain or flank pain.
Additional symptoms that may be associated with this disease:
Increased urinary frequency or urgency.
Passing large amounts of urine.
Urinating frequently at night.
Fever and chills.
The general diagnostic studies include a urinalysis (i.e., routine, microscopic), a complete blood cell count (CBC), a complete metabolic panel (CMP), and prothrombin time (PT) and activated partial thromboplastin time determinations. If patients have concomitant fever, obtain urine and blood cultures under sterile conditions. If patients are prostrate and obtunded, measure arterial blood gases (ABGs) and perform standard electrocardiography and chest radiography. If acute obstruction is suspected, perform renal ultrasonography or another radiographic evaluation and request an immediate consultation with an urologist.
The most common urinalysis findings include proteinuria, pyuria, bacteriuria, and low urine-specific gravity. More than 50% of patients develop leukocytosis and azotemia.
An acutely elevated serum creatinine may be the result of either a bilateral or unilateral process. This process can be obstructive or may be the manifestation of some toxic, metabolic, or inflammatory insult.
Patients with known or possible obstruction require an urgent consultation with an urologist.
If the clinical picture is suggestive, investigate for any of the conditions associated with renal papillary necrosis, including pyelonephritis, obstructed urinary tract, hemoglobinopathies, tuberculosis, liver cirrhosis, analgesic abuse, renal transplant rejection, and diabetes mellitus.
Clinical findings may also prompt performing hemoglobin electrophoresis, a subdermal tuberculin test, liver function tests, serum ammonium measurements, serum and urine salicylate and acetaminophen levels, a hemoglobin A1c measurement, and cyclosporin or tacrolimus levels.
Patients who present with hematuria, even if diagnostic interventions indicate papillary necrosis, require a full urologic workup for their hematuria because they may have a concomitant bladder tumor or similar lesion.
Because ischemia is such a prominent underlying factor in the development of renal papillary necrosis, promptly resuscitate patients and treat their hypoxia, if present. In addition, patients with acute disease may require broad-spectrum intravenous antibiotics, hydration, glycemic control, and urinary alkalinization. Cessation of analgesic abuse stabilizes and may improve renal function.
In patients without acute ureteral obstruction, treat the infectious and metabolic complications of renal papillary necrosis by replacing insensible losses, maintaining hydration, alkalinizing the urine, and administering antibiotics directed toward the pathogen (as revealed by culture or Gram stain and by observing for the development of obstruction or sepsis). Patients with hematuria significant enough to cause an acute drop in their hematocrit level may require blood transfusions. Patients with sickle cell disease (SCD) may require exchange transfusions, and patients with diabetes who have acute infectious complications and refractory hyperglycemia may require insulin therapy. Basically, ameliorate the ischemia with hydration and alkalinization, treat the underlying cause of the renal papillary necrosis (eg, maintain normal glycemic state), and institute targeted antibiotic therapy.
Acute obstruction with concomitant urinary tract infection is a urologic emergency that requires immediate percutaneous nephrostomy to relieve the obstruction, ureteral stent placement, or endoscopic retrieval of the obstructing sloughed papillae. Endoscopic retrieval is not recommended unless the offending papillae are crowning or extruding from the ureteral orifice; even then, the procedure is challenging. Retrograde pyelography and ureteroscopy are useful diagnostic tools, but consider these only when the patient is afebrile and after intravenous administration of antibiotics. Otherwise, a ureteral stent would suffice, delaying retrograde instrumentation until the patient is afebrile.
The recommended treatment is to drain the dilated collecting system either endoscopically or percutaneously. In patients with severe disease who are febrile and have smoldering sepsis, percutaneous nephrostomy is preferred because it does not require general anesthesia and carries a smaller risk of pyelovenous reflux and worsening sepsis. Cystoscopy and ureteral stent placement allow cystoscopic surveillance of the bladder, which is necessary if hematuria is the presenting symptom. However, in a patient with hydronephrosis, high fever, leukocytosis, and overt sepsis, the preferred treatment is to percutaneously drain the kidney. Perform diagnostic cystoscopy and RPGs (if necessary) later, when the patient's situation is not so dire.
NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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