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Renal papillary necrosis

Authors:
Stephen Geller at Vermont College of Fine Arts
Stephen Geller
Fernando Peixoto Ferraz de Campos at University of São Paulo
Fernando Peixoto Ferraz de Campos
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Abstract and Figures

In 1877, Dr. Nikolaus Friedreich (1825-1882; student of Virchow who became Professor of Pathology at Heidelberg and who also described Friedreich’s ataxia) first described renal papillary necrosis (RPN) in patients with prostatic hypertrophy and secondary hydronephrosis. Thereafter in 1937, Froboese and Günther emphasized the association of this entity with diabetes mellitus. These authors also observed renal papillary necrosis in cases of urinary tract obstruction even in the absence of diabetes mellitus.
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Copyright © 2013 Autopsy and Case Reports – This is an Open Access article distributed of terms of the Creative Commons Attribution Non-
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a Department of Pathology and Laboratory Medicine – Weill Medical College of Cornell University – New York – USA.
b Department of Internal Medicine – Hospital Universitário – Universidade de São Paulo, São Paulo/SP – Brazil.
Autopsy and Case Reports 2013; 3(4): 69-71
69
Renal papillary necrosis
Stephen A. Gellera, Fernando P. F. de Camposb
Geller SA, Campos FPF. Renal papillary necrosis. Autopsy Case Rep [Internet]. 2013; 3(4): 69-71. http://dx.doi.
org/10.4322/acr.2013.042
In 1877, Dr. Nikolaus Friedreich1 (1825-
1882; student of Virchow who became Professor
of Pathology at Heidelberg and who also described
Friedreich’s ataxia) rst described renal papillary
necrosis (RPN) in patients with prostatic hypertrophy
and secondary hydronephrosis. Thereafter in 1937,
Froboese2 and Günther3 emphasized the association
of this entity with diabetes mellitus. These authors
also observed renal papillary necrosis in cases of
urinary tract obstruction even in the absence of
diabetes mellitus.
In 1952, Mandel’s4 report corroborated the
latter ndings, suggesting that urinary tract infection
played a role in the pathogenesis of RPN. His
report showed the presence of urinary infection in
95% of cases of RPN, in autopsy studies. It was
in the late 1950s that analgesics emerged as a
major etiological factor of RPN.5 Since then some
series reported that analgesic abuse accounted
for 80 – 90% of cases of RPN.5-7 In this setting
non-steroidal anti-inammatory drugs (NSAID)
are also included with their incidence increasing
Figure 1 – Renal papillary necrosis. Irregularly round or oval areas of yellow necrosis are seen in renal
papilla and medullary areas of the kidney from a 62-year-old female with type 1 diabetes mellitus. A urinary
tract infection was also present as evidenced by the mildly inamed renal pelvis epithelium (acute pyelitis).
Picture provided by Dr. Stephen A. Geller - personal archive.
70
Autopsy and Case Reports 2013; 3(4): 69-71 Geller SA, Campos FPF.
reect as effects on vasculature, since medullary
interstitial cells synthesize prostaglandins. Studies
have also shown that ischemia results from direct
endothelial cell damage.15 Regardless the involved
mechanism, the end result is reduced prostaglandin
production, leading to decreased vascular perfusion,
vasoconstriction and eventually ischemic necrosis.8
The lack of specic symptoms, in the
early stages, makes diagnosis challenging. Later
clinical features include: nocturia, dysuria, pyuria,
hematuria (most notably microscopic hematuria),
ureteral colic, necrotic papillae voided in the urine6
and back pain. Renal function studies may also
reveal decreased glomerular ltration rate (GFR),
increased urea blood nitrogen (BUN) and renal
tubular acidosis. Eventually RPN leads to death or
chronic renal failure.8
Histologically, renal papillary necrosis is
characterized by coagulative necrosis of the renal
papilla and the background medullary pyramids.
Subsequently the necrotic foci can become infected
either from ascending cystitis or hematogenous
dissemination and be seen as acute liquefactive
necrosis with potential abscess formation. The
papilla, whether infected or not, can cause renal
tubular obstruction. Sloughed papilla can be seen in
cytopathology preparations of urine. In time brosis
and calcication occur. Bilateral involvement, or
involvement of a solitary kidney, can lead to renal
failure. If renal papillary necrosis is complicated by
infection can lead to death, particularly in the diabetic
patient who may or may not have other signicant
medical problems. Even in the non-diabetic patient,
renal papillary necrosis is potentially fatal.
As a last note, it has been suggested that
the rst description of RPN is in the record of
Beethoven’s autopsy.16 The translation of the
original Latin of the report says, “every one of their
calices was occupied by a calcareous concretion of
a wart-like shape and is large as a split pea.” In a
subsequent paper17, the wording of the translation
was changed to “every single calyx was lled with a
calcareous concretion like a pea which had been cut
across the middle.” In addition, the renal capsule is
described as a “cellular membrane of an inch thick,”
indicative of chronic renal inammation rather than
acutely occurring RPN. This may, instead of RPN,
be a description of extensive nephrolithiasis in
association with chronic pyelonephritis. When RPN
develops it is typically irregular and does not affect
“every single” papilla. Further the necrotic papilla
slough and break off, to be excreted, and evidence
would similarly not be present throughout. “Wart-
as these medications are more often utilized. The
risk highest is for phenacetin (no longer used in
many countries) and acetaminophen. In general,
the risk for analgesic nephropathy is cumulative.
More recently, it has been shown that these drugs
are harmful to human kidneys in the presence of
volume depletion, underlying renal disease as
well as long-term abuse.8 Other causes of RPN
include: sickle-cell hemoglobinopathies9,10, post-
renal transplants11, chronic liver disease12, shock
and severe dehydration, the latter mainly observed
during infancy.5
The principal causes are summarized in
Table 1.
Table 1 – Major causes of renal papillary necrosis
(RPN)
Analgesic nephropathy
Sickle cell nephropathy
Diabetes mellitus, often with urinary tract infection
Prolonged use of NSAIDs
An expanded list of causes is summarized
with the English language mnemonic “POSTCARDS”
(pyelonephritis, obstructive uropathy, sickle cell
disease, tuberculosis, chronic liver disease,
analgesic/alcohol, renal transplant rejection, diabetes
mellitus, systemic vasculitis).13
The frequency of RPN in different disease
conditions is unknown because of underdiagnosed
pauci- or asymptomatic cases. However
approximately 30% of all cases of RPN occur in
the setting of diabetes mellitus. In these cases,
hyperglycemia is usually uncontrolled, and urinary
tract infections are frequently seen. The relationship
of RPN with diabetic microangiopathy could be
demonstrated either in vivo or in an autopsy series.14
Friedreich5 proposed a vascular mechanism
to explain the RPN regardless of underlying disease.
Unequivocally, this mechanism is observed in sickle
cell disease, where vasa recta are obstructed by
the sickling erythrocytes. In case of analgesics
and NSAID, ischemia can be demonstrated in the
medulla and vasa recta due to direct inhibition
of cyclooxygenase-mediated production of
prostaglandins.8 A direct toxic effect on cells of
the medulla is also involved in the pathogenesis
of RPN. Damage to these cells may similarly
71
Renal papillary necrosis Autopsy and Case Reports 2013; 3(4): 69-71
6.
Harvald B. Renal papillary necrosis. A clinical survey of
sixty-six cases. Am J Med. 1963;33:481-6. http://dx.doi.
org/10.1016/0002-9343(63)90147-5
7.
Hultengren N. Renal papillary necrosis. A clinical study of
103 cases. Acta Chirurg Scand. 1961;277:1-84.
8.
Brix AE. Renal papillary necrosis. Toxicol Pathol. 2002;30:672-
4. http://dx.doi.org/10.1080/01926230290166760
9.
Harrow BR, Sloane JA, Liebman NC. Roentgenologic
demonstration of renal papillary necrosis in sickle cell trait.
N Engl J Med. 1963;268:969. PMid:13953018. http://dx.doi.
org/10.1056/NEJM196305022681802
10.
Voulgarelis M, Ziakas P. Renal papillary necrosis unmasking
sickle cell disease. N Engl J Med. 2005;352:1237.
PMid:15788500. http://dx.doi.org/10.1056/NEJMicm030682
11. Edmondson RPS, Fawcet TW, Jones NF, Cade R, Tarrant
DG, Juncos LI. Papillary necrosis in a transplanted kidney. Br
Med J. 1972;1:547. http://dx.doi.org/10.1136/bmj.1.5799.547
12.
Edmondson HA, Reynolds TB, Jacobson HG. Renal papillary
necrosis with special reference to chronic alcoholism. Arch
Intern Med. 1966:118:255. PMid:5947305. http://dx.doi.
org/10.1001/archinte.1966.00290150069013
13.
Powell C, Donohoe JM, Mydlo JH. Papillary necrosis [Internet].
Medscape; 2012. [cited 2013 Oct 2]. Available from: http://
emedicine.medscape.com/article/439586-overview#a0102
14.
Groop L, Laasonen L, Edgren J. Renal papillary necrosis
in patients with IDDM. Diabetes Care. 1989;12:198-202.
http://dx.doi.org/10.2337/diacare.12.3.198
15.
Wolf DC, Turek JJ, Carlton WW. Early sequential ultrastructural
renal altrations induced by 2-bromoethylamine hydrobromide
in the Swiss ICR mouse. Vet Pathol. 1992;29:528-35. http://
dx.doi.org/10.1177/030098589202900607
16.
Schwarz A. Beethoven’s renal disease based on his autopsy:
a case of papillary necrosis. Am J Kid Dis. 1993;21:643-52.
PMid:8503419.
17.
Davies PJ. Beethoven’s nephropathy and death: discussion
paper. J Roy Soc Med. 1999;86:159-61.
like,” the descriptive term used, is not likely to be
RPN, and, although color descriptors appear in
other parts of the report, there is no use of “yellow,”
typical of necrosis, in the kidney section. The
pathologist, Johann Wagner, was experienced and
highly regarded, including by his student Karl von
Rokitansky, developer of the great Viennese school
of pathology. As was the custom of the time the
report concentrates on explaining clinical problems
and the prostate gland, likely enlarged in a 57 year
old man and possibly the cause of at least partial
obstruction and subsequent pyelonephritis, is not
mentioned. In addition it is highly unlikely that he
would have mistaken the papilla for a calyx, since
the anatomy of the kidney had been well described
by Marcello Malpighi (1628-1694) two centuries
before.
Keywords: Kidney Papillary Necrosis;
Diabetes Mellitus; Urinary Tract Infections; Anti-
inammatory Agents, Non-Steroidal.
REFERENCES
1.
Friedreich N. Über Necrose der Nierenpapillen bei
Hydronephrose. Virchows Arch Pathol Anat. 1877;69:308-
12. http://dx.doi.org/10.1007/BF02326121
2.
Froboese C. Uber sequestrierende Marknekrosen der
Nieren bei Diabetes Mellitus. Verh Deutsch Ges Pathol.
1937;30:431-43.
3.
Guenther GW. Die Papillennekrosen der Niere bei Diabetes.
München Med Wschr. 1937;84:1695.
4.
Mandel EE. Renal medullary necrosis. Am J Med.
1952;13:322-7. http://dx.doi.org/10.1016/0002-9343(52)90286-
6
5.
Renal papillary necrosis. Lancet. 1982;320:588-90. http://
dx.doi.org/10.1016/S0140-6736(82)90665-1
Stephen A. Geller, M.D.
Department of Pathology and Laboratory Medicine
Weill Medical College of Cornell University
New York - USA
geller16st@gmail.com
Fernando P. F. de Campos, PhD
Department of Internal Medicine
Hospital Universitário - USP
São Paulo/SP - Brazil
fpfcampos@gmail.com
... Papillary necrosis has been described in analgesic nephropathy, urinary tract infection, sickle cell disease, uncontrolled diabetes mellitus, calyceal arteritis, and necrotizing angiitis. 2 Candida-associated renal papillary necrosis is very rarely reported in the literature. Growth of Candida in urine culture in a patient with diabetes mellitus is often neglected as it is thought to reflect contamination. ...
... Infected papillary necrosis may be fatal. 2 Candida-associated renal papillary necrosis was first described in 1981. 9 The primary reported association was immunosuppression due to drugs or extreme prematurity in infants. ...
Candida-Associated Renal Papillary Necrosis Following Severe COVID-19 Infection
Article
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  • Apr 2024
Candida-associated renal papillary necrosis is rare. The few cases described previously were secondary to candidemia, especially in immunocompromised hosts. We describe two patients who presented with hydroureteronephrosis and were diagnosed with candida-associated renal papillary necrosis. Both patients had a history of severe COVID-19 infection within the past year and had been treated with immunosuppressants. Both patients underwent double J stenting and anti-fungal treatment with fluconazole. One patient recovered completely, while the other patient who had chronic kidney disease stage 4 at diagnosis progressed to dialysis-dependent renal failure later following an episode of bacterial sepsis. The incidence of candida-associated renal papillary necrosis may reflect the immunomodulatory effects of COVID-19, immunosuppressants, or a combination of both.
View
... Ischemic biological necrobiosis of the papilla in the medulla of the kidneys causes cell death of the renal medullary pyramids and papillae. The hallmark of the disease is coagulative necrosis of the renal medullary pyramids and papillae secondary to multiple conditions (POST-CARDS) and toxins [24]. Most patients who present with papillary necrosis have at least two contributing risk factors, and necrosis can involve one or up to 18 papillae [25]. ...
... This also raises concerns regarding the high caffeine content in energy drinks meant to assist with high endurance and keeping people awake. Nonetheless, indication of analgesics as a major etiological factor of RPN has long been described (1950s) with 80-90% of RPN cases attributed to AN [24]. Previous studies report an increased number of RPN cases in people who abuse aspirin, with some studies describing paracetamol AN, caused by the main metabolite phenacetin. ...
Renal Papillary Necrosis (RPN) in an African Population: Disease Patterns, Relevant Pathways, and Management
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  • Dec 2022
Renal papillary necrosis (RPN) is characterized by coagulative necrosis of the renal me-dullary pyramids and papillae. Multiple conditions and toxins are associated with RPN. Several RPN risk factors, or POSTCARDS, have been identified, with most patients presenting with RPN having at least two contributing risk factors. Currently, there is no specific test to diagnose and confirm RPN; however, several imaging tools can be used to diagnose the condition. RPN is currently underdiagnosed in African populations, often with fatal outcomes. In African clinical settings , there is a lack of consensus on how to define and describe RPN in terms of kidney anatomy, pathology, endourology, epidemiology, the identification of African-specific risk factors, the contribution of oxidative stress, and lastly an algorithm for managing the condition. Several risk factors are unique to African populations including population-specific genetic factors, iatrogenic factors, viral infections, antimicrobial therapy, schistosomiasis, substance abuse, and hypertension (GIVASSH). Oxidative stress is central to both GIVASSH and POSTCARDS-associated risk factors. In this review, we present information specific to African populations that can be used to establish an updated consensual definition and practical grading system for radiologists, urologists, neph-rologists, nuclear physicians, and pathologists in African clinical settings.
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... Renal papillary necrosis histologically is marked by coagulative necrosis of the renal papilla and the medullary pyramids. This can lead to fibrosis and calcification and eventually to renal failure (67). In preclinical safety testing, renal papillary necrosis is a relatively common form of toxicity encountered, also being encompassed under the term analgesic nephropathy (55). ...
... Even though renal papillary necrosis risk can effectively be determined through the measurement of monoclonal antibodies to rat renal papillary tissue (RPA-1 and RPA-2) in the urine of laboratory rats, histopathology is the commonly used method in routine toxicology testing for identification of renal papillary necrosis in rats (55). In human patients main causes for this type of necrosis include analgesic nephropathy (69,70), the prolonged use of NSAIDs (71), sickle cell nephropathy (72,73), as well as diabetes mellitus (67). ...
Analysis of the Frequency of Kidney Toxicity in Preclinical Safety Studies using the eTOX Database
Thesis
Full-text available
  • Jan 2022
This research aimed to obtain reliable data on the frequency of different types of renal toxicity findings in 28-day oral gavage studies in Wistar rats, their consistency across species and study duration, as well as the correlation between histopathological endpoints and routinely used clinical chemistry parameters indicative of kidney injury. Analysis of renal histopathological findings was carried out through extraction of information from the IMI eTOX database. Spontaneous renal histopathological findings in 28-day oral gavage studies in control Wistar rats and beagle dogs confirmed tubular basophilia and renal dilation as the most frequent incidental findings in controls, whereas necrosis and glomerulosclerosis were not identified at all or only rarely as a background lesion. Histopathological evidence of necrosis and glomerulosclerosis was associated with changes in clinical chemistry parameters in 28-day oral gavage Wistar rat studies. Necrosis was frequently accompanied by a statistically significant rise in serum creatinine and serum urea, whereas serum albumin was frequently found to decrease statistically significantly in treatment groups in which necrosis was recorded. In contrast to necrosis, glomerulosclerosis was not associated with statistically significant changes in serum creatinine and urea in any of the 28-day oral gavage Wistar rat treatment groups, but appears to be best reflected by a pattern of statistically significantly lowered serum albumin and serum protein together with a statistically significant increase in serum cholesterol. As might have been expected based on the high background incidences of tubular basophilia and dilation, no consistent changes in any of the clinical chemistry parameters were evident in animals in which renal lesions were con� fined to renal tubular basophilia or dilation. In summary, the routinely provided clinical chemistry parameters are rather insensitive - novel kidney biomarkers such as Cystatin C, β-trace protein and Kidney injury molecule 1 should further be evaluated and integrated into routine preclinical and clinical practice. However, evaluation of clinical chemistry data was limited by the lack of individual animal data. Even though an extensive amount of preclinical studies is accessible through the eTOX database, comparison of consistency across time was limited by the limited number of shorter- and longer term studies conducted with the compounds identified as causing renal histopathological changes within a 28- day study in rats. A high consistency across time for both treatment-related tubular basophilia and treatment-related dilation cannot be confirmed for either of the two effects as these two findings were both induced only rarely in studies over a different treatment-duration other than 28 days after administration of the compounds which provoked the respective effect in a 28-day study. For the finding of necrosis consistency across time was low with the exception of “AZ_GGA_200002321”, in which renal papillary necrosis was identified consist� ently throughout different treatment durations (2, 4, 26, 104 weeks). No shorter and longer-term studies were available for the compounds identified as causing glomerulosclerosis within a 28-day study in rats. No consistent findings of the selected histopathological endpoints were identified in any of the corresponding 28-day oral gavage beagle dog studies after treatment with the identical compounds, which caused the respective ef� fect after 28-day treatment in rats. However, in the overwhelming majority of cases, beagle dogs were administered lower doses in these studies in compar� ison to the corresponding 28-day Wistar rat studies. Searching the eTOX database yielded no 28-day oral gavage studies in Wistar and Wistar Han rats in which accumulation of hyaline droplets, tubular atrophy or hyperplasia was recorded. Only one 28-day oral gavage Wistar rat study was identified with the histopathological result of neutrophilic inflammation. Consequently, evaluation of these four renal findings in relation to clinical chemistry parameters and consistency across time and species cannot be made. In summary, this work contributes knowledge through mining and evaluating the eTOX database on a variety of specific renal endpoints that frequently occur after administration of trial substances in 28-day oral gavage studies in Wistar rats in the field of preclinical toxicity with specific focus on their frequency relation to background findings, as well as consistency across time and species. Targeted statistical evaluation of in vivo data within joint research ventures such as the eTOX project, presents an enormous opportunity for an innovative future way of aiding preclinical research towards a more efficient research in the preclinical stage of drug development. This could be achieved through the aug� mentation of methodological strategies and possibly novel software tools in order to predict in vivo toxicology of new molecular entities by means of information that is already available before early stages of the drug development pipeline begin.
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... Pyelonephritis, diabetes mellitus, liver cirrhosis, urinary tract infection are other causes [2,5,8]. In humans approximately 30% of all cases of renal papillary necrosis occur due to diabetes mellitus [6]. ...
... According to Dr. Johann Wagner who performed autopsy of Ludwig van Beethoven (Beethoven's case appears to be the first report of renal papillary necrosis), symmetrical soft calyceal concretions (containing mainly ammonium magnesium phosphate) and their appearances are typical lesions for diagnosis of renal papillar necrosis [4,6]. Although the mentioned typical concretions of papilla were not macroscopically observed in our case, the presence of crystals in the tubule lumen and the formation of struvite stone (which has the same chemical composition with calyceal concretions) established a distinct relationship between urolithiasis and renal papillary necrosis. ...
Pathological Changes of Urinary System in a Dog with Urolithiasis and Renal Papillary Necrosis
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Background: Urolithiasis is one of the important lower urinary tract diseases in dogs. Uroliths develop when urine becomes
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... These papillary fragments can cause ureteral obstruction which requires immediate intervention. [9] The differential diagnosis of GN is very broad and complex. Based on the clinical presentation the above patient is presenting with a nephritic syndrome with rapid progression (rapidly progressive GN). ...
Challenges in Diagnostic and Management of Nephritic Syndrome in Diabetic Nephropathy Patient: a Case Report
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  • May 2021
The clinical presentation of patients with acute glomerulonephritis (GN) varies widely, from asymptomatic to clinical presentations of acute kidney injury (AKI), edema, and hypertension. Diagnosis of GN in patients with diabetic nephropathy (DN) is a challenge due to pre-existing edema, hypertension, and decreased renal function. Likewise in terms of management of steroid immunosuppressants related to blood sugar regulation. It has been reported that 35-year-old male patients with diabetes mellitus (DM) with DN whose kidney function deteriorated rapidly. The patient complained of cola-red urine and decreased urine volume the day before admission. Physical examination showed blood pressure of 160/95 mmHg, bilateral leg edema, active chronic ulcer in the left lower leg, hemoglobin level was 8.7 g / dl, leukocytes 17.400 / ul, serum urea level 96 mg / dl, serum creatinine level 7.01 mg / dl (baseline level was 2.3 mg / dl), ASTO titer + 800 IU / ml, macroscopic hematuria, and albuminuria +4 on urinalysis. Ultrasonography revealed enlarged kidney size and signs of acute renal inflammation. Based on these data the patient was diagnosed clinically as rapidly progressive GN due to post-infectious GN. The patient received 3 days of pulse methyl prednisolone therapy continued orally, blood sugar regulation with insulin, RAS blockers, intravenous antibiotics and ulcer debridement. After 1 week of therapy, clinical and laboratory improvements were found and at the next followup renal function returned to baseline about 2 weeks later.
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... In the more rare events of RPN in the pediatric population, it is more likely to be caused by sickling crises in SCD. Approximately 30% of all cases of RPN are likely due to patients with diabetes mellitus; however, the overall frequency and prevalence is unclear because of underdiagnosis of many asymptomatic cases [6]. Similarly, it is estimated that the incidence of RPN due to SCD is 30-40%, though this etiology may also be underdiagnosed [7]. ...
Renal Papillary Necrosis Following Mesenteric Artery Stenting
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  • Oct 2020
A 62-year-old man presented with left flank pain and hematuria four days after undergoing mesenteric artery balloon angioplasty and stent placement. Imaging revealed left renal infarction with associated papillary necrosis and a thrombus in the left collecting system causing acute renal obstruction. Complete obstruction was confirmed using MAG3 Renal Scan with Lasix. A nephrostomy tube was inserted under CT guidance by interventional radiology with complete resolution of obstruction and hematuria.
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... In humans, diabetes mellitus is the most common cause of renal papillary necrosis. Sickle cell haemoglobinopathy, chronic pyelitis, urinary tract obstruction or infection and long-term use of NSAIDs are associated with renal papillary necrosis (Geller and de Campos 2013). In exotic felids, renal papillary necrosis is most commonly associated with NSAID toxicosis or dehydration and occasionally with pyelitis (Newkirk et al. 2011). ...
Urocystitis, pyelonephritis, renal papillary necrosis and chronic tubulointerstitial disease causing chronic renal insufficiency in a Siberian tiger (Panthera tigris altaica): a case report
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Full-text available
  • Oct 2018
The present case report describes a case of chronic renal failure characterised by renal medullary fibrosis and renal papillary necrosis in a male Siberian tiger (Panthera tigris altaica). A 12-year-old male Siberian tiger presented with depression, anorexia and weight loss. Blood urea nitrogen (> 50.4 mmol/l) and ammonia (71.7 µmol/l) were increased, suggesting chronic renal failure and uraemia. The tiger died secondary to gastric haemorrhage. At necropsy, the kidneys had yellow lesions in the medulla and renal papillae and petechiae in the cortex. The stomach had multiple mucosal ulcers and haemorrhage. Microscopically, marked renal medullary fibrosis and renal papillary necrosis were observed with tubular atrophy, degeneration, coagulative necrosis, calcification and chronic inflammatory cell infiltration. The renal cortex showed moderate interstitial inflammation. The urinary bladder exhibited epithelial desquamation and submucosal fibrosis. The tiger was diagnosed with chronic renal failure secondary to renal papillary necrosis and medullary fibrosis.
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Acute kidney injury associated with non-steroidal anti-inflammatory drugs
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  • May 2022
  • EUR J INTERN MED
Non-steroidal anti-inflammatory drugs (NSAIDs) are ones of the commonly prescribed drugs worldwide. They primarily inhibit cyclooxygenase (COX) enzyme which is responsible for conversion of phospholipids to various prostaglandins (PGs). Disruption in PGs production affects the kidneys in several ways, including vasoconstriction that may result in ischemic acute kidney injury (AKI) in at-risk patients. They also impair salt and water excretion, leading to edema and hypertension. Other complications include hyperkalemia, hyponatremia, nephrotic syndrome, acute interstitial nephritis and chronic kidney disease progression. AKI from NSAIDs is usually reversible with favorable prognosis after discontinuation of NSAIDs. Avoidance of NSAIDs exposure is extremely important, especially among high-risk patients.
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Haematuria in adults
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  • Mar 2022
Haematuria in adults is a common complaint, whether it be visible (macroscopic, previously called frank) haematuria or non-visible (microscopic) haematuria and may be either symptomatic or asymptomatic. Haematuria is a non-specific symptom generated by a wide range of medical and surgical causes. Determining the cause requires thorough history, examination and investigation. Visible haematuria and symptomatic non-visible haematuria always require investigation.
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Renal Papillary Necrosis With Special Reference to Chronic Alcoholism
Article
  • Sep 1966
  • ARCH INTERN MED
IN recent years, in a study of the clinical and pathological aspects of liver disease in patients with chronic alcoholism, it was observed that acute renal failure due to papillary necrosis occurred in a significant number. None of the patients had diabetes mellitus, urinary tract obstruction, or a history of excessive use of analgesics. In a search of the literature, only five examples of the concomitant occurrence of cirrhosis and papillary necrosis were noted. Knutsen et al1 mentioned that cirrhosis was present in one of 16 cases of papillary necrosis, all proven either at autopsy or in surgical specimens. Cirrhosis was mentioned as being present at autopsy in two of 14 cases of the sclerotic type of papillary necrosis reported by Schourup.2 In reports of the other two patients, an elevated blood-glucose level was mentioned, so that diabetes mellitus could not be ruled out. One was an elderly
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Renal medullary necrosis
Article
  • Sep 1952
  • AM J MED
Patients with diabetes and/or obstruction of the urinary tract and infection are predisposed to inflammation progressing to ischemic necrosis of the renal medulla, a life-threatening disease which has been described under the terms necrotizing papillitis, papillary necrosis and necrotizing pyelonephritis but here designated renal medullary necrosis. The present study is based on analysis of six patients and a review of the clinical and experimental literature on renal medullary necrosis. A concept of the disease has been developed which emphasizes infection as the common denominator. The pathologic disorder of medullary necrosis is viewed as an uncontrolled infection, compromised by local vascular tissue factors and by defective resistance on the part of the host. Demonstration of this lesion on biopsy in a previously anuric patient suggests a prenecrotic phase of the disease which may be reversible with prompt antibiotic therapy.
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Early Sequential Ultrastructural Renal Alterations Induced by 2-Bromoethylamine Hydrobromide in the Swiss ICR Mouse
Article
  • Dec 1992
Thirty-two male Swiss ICR mice were injected intraperitoneally with 300 mg 2-bromoethylamine hydrobromide/kg body weight, anesthetized, and perfused with glutaraldehyde-paraformaldehyde solution at 5, 15, 30, 60, 90, 120, 150, and 180 minutes after treatment. Eight control mice were injected intraperitoneally with sterile diluent, and one was perfused at each of the same time periods as the treated mice. Proximal tubule epithelial alterations progressed over time from increased secondary lysosome and myeloid body formation to cellular and mitochondrial swelling and eventually cell necrosis. The glomerular, peritubular, and vasa recta capillaries had endothelial cell swelling and desquamation and platelet aggregation. Bromoethylamine nephrotoxicosis in the male Swiss ICR mouse is an ischemic necrosis of the proximal tubules and papilla initiated by endothelial cell damage and makes an excellent model of chemically induced damage to endothelial cells and tubular necrosis.
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Renal Papillary Necrosis in Patients With IDDM
Article
  • Apr 1989
  • DIABETES CARE
Although diabetes mellitus is reported in 29% of patients with renal papillary necrosis (RPN), the frequency of RPN among patients with insulin-dependent diabetes mellitus (IDDM) has from autopsy studies been estimated to be only 4.4%. In vivo data on the prevalence of RPN in patients with IDDM have been lacking. We therefore studied the prevalence of RPN in 76 patients with long-standing IDDM and in 34 age-matched control subjects by intravenous urography. None of the control subjects showed radiographic signs of papillary necrosis. RPN was observed in 18 patients (23.7%); 15 were women (83.3%). Age and duration of diabetes was not different between patients with and without papillary necrosis, and there was no significant difference between the two groups regarding the prevalence of microangiopathic complications, i.e., proliferative retinopathy and diabetic nephropathy. Microscopic hematuria was three times more frequent in patients with than without RPN (44 vs. 16%; P less than .02). In addition, pyuria was reported in 40% of patients with papillary necrosis, and 61% of them gave a positive history of urinary tract infection compared to 16% (P less than 05) and 32% (P less than .02), respectively, in patients without papillary necrosis. It is concluded that RPN is a more frequent complication of long-standing IDDM than appreciated from autopsy studies, and being female and having a history of urinary tract infection are associated with an increased risk of RPN.
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