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Introduction:
Renal papillary necrosis is not commonly seen in daily practice, but can have severe consequences when it is not diagnosed in time. It is known to be associated with sickle cell hemoglobinopathies; however a wide range of etiologies are possible, and it is therefore not the first diagnosis clinicians consider in patients with sickle...
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Context 1
... hematuria is the presenting symptom of RPN, pa- tients require a full diagnostic workup. Fig. 5 shows a flowchart for clinical evaluation of gross hematuria in pe- diatric patients based on the ESPU Pediatric Urology Web- book [22]. The hematuria should only be attributed to RPN when all other results are negative; excluding all other possible causes [20]. Therefore a guideline directed eval- uation of gross hematuria should be performed. The clinical evaluation in gross hematuria should start with a good history and clinical examination. The laboratory in- vestigations consist of a urine culture and sensitivity, complete blood count (CBC), urea and electrolytes (U&E), complement C3, CRP, spot urine (calcium/creatinine ratio, 24-h urine volume and calcium excretion), renal ultra- sound, and considering investigating the parents [22]. As SCD is a chronic disease, there is a substantial risk of chronic kidney disease and therefore medical workup with assessment of the renal function is important and when abnormal the patient should be referred to a pediatric nephrologist. However, when an anomaly of the urinary tract is suspected the patient should be referred to a pe- diatric urologist and additional imaging is required. The upper urinary tract must be evaluated by imaging study with intravenous contrast if possible. To diagnose RPN in adults, a contrast material-enhanced CT during the excre- tory phase is now the gold standard, because it can help to identify RPN at an early stage. This is because it shows the full range of specific features better than intravenous urography (IVU), RPG, and ultrasound, which were used to diagnose RPN in the past (Figs. 1e4) [8,23]. It is recom- mended that these imaging studies are performed before cystoscopy, so that in case of the imaging studies giving an incomplete result, the urologist can perform a bilateral RPG during cystoscopy. In adults who present with hematuria, a cystoscopy can be performed under local anesthesia; however, pediatric patients require general anesthesia. This lowers the threshold to perform a RPG at the same time. Finally a ureterorenoscopy (URS) may be necessary to assess the ureter or collecting system when a filling defect is visible on RPG. It is important to note that interventional retrograde studies (RPG and URS) are only performed when there is no acute obstruction with possible pyonephrosis, because they can exacerbate sepsis. It is mandatory that precautions, antibiotics, and slow introductions of the contrast are taken before doing an RPG ...
Context 2
... hematuria is the presenting symptom of RPN, patients require a full diagnostic workup. Fig. 5 shows a flowchart for clinical evaluation of gross hematuria in pediatric patients based on the ESPU Pediatric Urology Webbook [22]. The hematuria should only be attributed to RPN when all other results are negative; excluding all other possible causes [20]. Therefore a guideline directed evaluation of gross hematuria should be ...
Citations
... The drug which causes acute interstitial nephritis is penicillin, ciprofloxacin, loop diuretics, etc. [71]. Papillary necrosis is a condition in which excess consumption of analgesiccontaining phenacetin causes necrosis of renal papillae [72]. Glomerular injury is a very rare condition that may be caused due to drugs like ampicillin, rifampin, and phenytoin. ...
Chronic kidney disease (CKD) is one of the most outgrowing diseases of all, and globally, about 10% of the world's population is affected. Chronic kidney disease (CKD) occurs when the kidney can no longer perform its function to full capacity. There are currently two treatment options for CKD: dialysis and transplantation. Both existing treatment options have their demerits, including high cost, pain, sleep disturbances, restlessness, graft rejection, and much more. Zingiber officinale, also commonly known as ginger, is one of the most commonly used household herbs and a potential medicinal herb. It contains various phytochemicals such as essential oils, phenolic compounds, alkaloids, glycosides, flavonoids, terpenoids, saponin, tannin, protein, and carbohydrates. Ginger has been reported for multiple medicinal properties such as antibacterial, antioxidant, anti-inflammatory, immune-modulatory, anti-hypertensive, anti-arthritic, hepatoprotective, and nephroprotective. The nephroprotective properties of ginger are less explored than their other therapeutic properties. Few research data suggest that the aqueous extracts of ginger lowered blood glucose, serum, urea, and creatinine levels in diabetic-induced rats. It also helped to restore the changes in the kidney due to toxicity. Thus, it protects renal tissues from structural damage caused by hypoglycemia, inhibits cholesterol absorption due to oxidative stress, and also boosts the kidney's defense mechanism. The in silico work performed on 64 phytochemicals against the Vitamin D3 receptor target protein of CKD showed the binding efficiency of phytochemicals against this target. Diterpene (Lactone) has shown a better binding score with optimal ADMET properties. Ginger compress therapy is a very simple treatment process, using pieces of ginger boiled in hot water, after which a towel is soaked in this ginger water and spread over the lower portion of the patient's back for around 30 minutes. After this, the area must be rubbed with a few drops of gingelly oil. Currently, many Siddha and Ayurveda practitioners in India and many other countries use this therapy to cure numerous patients. Deeper research into this therapy could enhance efficiency and provide a scientific approach.
... The renal papillae are considered to be anatomically vulnerable to ischemia, which may be seen in diabetes-associated vascular disorder, or interstitial edema secondary to infection[1]. There have been some cases, in which rapid deterioration occurred and even progressed to death [3]. The early treatment of RPN is important for improving prognosis and reducing morbidity. ...
Background:
Renal papillary necrosis (RPN) is a rare disease. It is difficult to distinguish RPN with urinary tract obstruction from upper urinary tract occupying lesions. We reported a case of RPN and made a definite diagnosis largely based upon its endoscopic characteristics.
Case summary:
A 75-year-old woman presented with right flank pain, visible hematuria and a body temperature greater than 39 ℃. Laboratory investigations revealed leukocytosis with 12.7 × 10/L white blood cells and 93.6% neutrophils. Blood creatinine was 333 umol/L. Ultrasonography showed hydronephrosis of the right kidney and a right distal ureteric lesion. After urgent placement of right ureteral double J stent and treatment with antibiotics, the patient's symptoms and the blood abnormalities improved rapidly. Computed tomography urography showed the presence of multiple occupying lesions in the right pelvis. The endoscopic ureteroscopy revealed that renal papillary necrosis and the subsequent migration of sloughed papillae into the upper ureter and calyces. The sloughed papillae appeared like "cottons", which were whitish, soft, and irregularly-shaped without blood supply. In addition, the necrotic and sloughed renal papillae were removed by flexible ureteroscopy to prevent further obstruction. Pathological examination found that infarcted renal papillae were associated with inflammatory exudation. Three months after discharge, follow-up computed tomography urography showed no obvious lesions in the renal pelvis.
Conclusion:
This case revealed the endoscopic features of RPN. In addition, flexible ureteroscopy proves to be vital in diagnosis and treatment of RPN.
... detected by imaging, as was the case with our patient. Management is dependent on the severity of hematuria and includes IV hydration and alkalinization of the urine, and exchange blood transfusions when occurring with sickle cell disease (2). The use of desmopressin, aminocaproic acid, and embolization or balloon tamponade have been described in case reports but have not been formally studied (3)(4)(5). ...
... Urinary stones are the most common cause of renal pelvis rupture [8] . Akpinar et al [9] described 91 patients April 16, 2021 Volume 9 Issue 11 parenchyma rupture (Table 3) [11][12][13][14] . Zhang et al [15] summarized 165 patients with spontaneous repair of the renal parenchyma from 1985 to 1999 and found that tumor was the main cause, accounting for 61.5% of patients, while the vasculature accounted for 17% of patients and infection accounted for 2.4% of patients. ...
Background:
Spontaneous renal rupture is a rare disease in the clinic. The causes of spontaneous renal rupture include extrarenal factors, intrarenal factors, and idiopathic factors. Reports on infection secondary to spontaneous renal rupture and the complications of spontaneous renal rupture are scarce. Furthermore, there are few patients with spontaneous renal rupture who present only with fever.
Case summary:
We present the case of a 52-year-old female patient who was admitted to our hospital. She presented only with fever, and the cause of the disease was unclear. She underwent a contrast-enhanced computed tomography (CT) scan, which showed that the left renal capsule had a crescent-shaped, low-density shadow; the perirenal fat was blurred, and exudation was visible with no sign of calculi, malignancies, instrumentation, or trauma. Under ultrasound guidance, a pigtail catheter was inserted into the hematoma, and fluid was drained and used for the bacterial test, which proved the presence of Klebsiella pneumoniae. Two months later, abdominal CT showed that the hematoma was absorbed, so the drainage tube was removed. The abdominal CT was normal after 4 mo.
Conclusion:
Spontaneous renal rupture due to intrarenal factors causes a higher proportion of shock and is more likely to cause anemia.
... These causes are usually not encountered in children. 3,10 We ruled out all these causes by history, examination and appropriate investigations. ...
In sickle cell disease (SCD), the clinical manifestations are due to episodes of vascular occlusion and haemolysis. Most of the children experience vaso-occlusive pain episodes by the age of six years. Renal injury in sickle cell disease referred to as sickle cell nephropathy is a frequent yet under-recognised complication. Renal papillary necrosis (RPN) as the first presentation in SCD is rare. We are reporting a 12 year old child with no prior vaso-occlusive episodes, presenting with renal papillary necrosis due to Sickle Beta and Thalassemia.
... RPN may be caused by surgical interventions as well as diseases of vasculature (systemic vasculitides), autoimmunity, hemoglobinopathy (e.g. sickle cell disease [SCD]/trait), pyelonephritis, diabetes mellitus, urinary tract obstruction, tuberculosis, renal vein thrombosis, tubulointerstitial nephritis, cirrhosis of the liver, and transplant rejection, as well as induced by substances such as in the case of analgesic and alcohol abuse [3,4]. RPN typically affects adults (>60 years of age) and is bilateral in 70% of cases [5]. ...
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.
... Papillary necrosis is a condition in which the tips of the renal pyramids or the renal papillae become ischemic and then necrotic. Predisposing factors include conditions in which the blood supply to the naturally hypoxic renal medulla may be compromised, such as diabetes mellitus and sickle cell anemia [13]. Papillary necrosis has also been observed in patients taking long-term high-dose anti-inflammatory medication (analgesic nephropathy) and in patients with urinary tract infections (including tuberculosis) and urinary tract obstruction [14]. ...
... The diagnosis is best made on excretory phase coronal reformatted CT images viewed at wide windows ( Fig. 6) [16]. On early enhanced images, the necrotic papillae are sometimes identified as small triangular-shaped hypoenhancing regions in the renal medulla [13]. ...
... Renal papillary necrosis is an infrequent pathology, which has been etiologically related to an infection of the renal pyramids associated with renal vasculopathy or obstruction of the upper urinary tract. Patients with diabetes, sickle cell anemia, chronic alcoholism and vascular disease are especially susceptible to this complication [2]. Even though tests such as urinary sediment (where papillary fragments can be observed) or culture (to check for the presence of infection) are important for the diagnosis, its basis will be made with imaging tests. ...
... Regarding the treatment of papillary necrosis, you should always focus on controlling the underlying disease, such as blood glucose levels, infection, correct hydration, or withdrawing analgesics [1,2]. ...
... Although water restriction activated NFAT5 and increased AQP2 in the inner medulla of SCD mice, it did not elevate urinary osmolality to the same degree as it did in non-SCD mice. One possibility is that the SCD mice may have small papilla, which reduce power of urine concentration, since SCD was shown to induce renal papillary necrosis (Henderickx et al. 2017). Thus, we examined the effect of SCD on the size of the papilla. ...
Sickle cell disease (SCD)‐induced urinary concentration defect has been proposed as caused by impaired ability of the occluded vasa recta due to red blood cell sickling to serve as countercurrent exchangers and renal tubules to absorb water and solutes. However, the exact molecular mechanisms remain largely unknown. The present studies were undertaken to determine the effects of SCD on vasopressin, aquaporin2 (AQP2), urea transporter A1 (UTA1), Na‐K‐Cl co‐transporter 2 (NKCC2), epithelial Na channels (ENaC), aquaporin1 (AQP1), nuclear factor of activated T cells 5 (NFAT5) and Src homology region‐2 domain‐containing phosphatase‐1 (SHP‐1), an important regulator of NFAT5, in the Berkeley SCD mouse kidney medulla. Under water repletion, SCD only induced a minor urinary concentration defect associated with increased urinary vasopressin level alone with the well‐known effects of vasopressin: protein abundance of AQP2, UTA1 and ENaC‐β and apical targeting of AQP2 as compared with non‐SCD. SCD did not significantly affect AQP1 protein level. Water restriction had no further significant effect on SCD urinary vasopressin. NFAT5 is also critical to urinary concentration. Instead, water restriction‐activated NFAT5 associated with inhibition of SHP‐1 in the SCD mice. Yet, water restriction only elevated urinary osmolality by 28% in these mice as opposed to 104% in non‐SCD mice despite similar degree increases of protein abundance of AQP2, NKCC2 and AQP2‐S256‐P. Water‐restriction had no significant effect on protein abundance of ENaC or AQP1 in either strain. In conclusion, under water repletion SCD, only induces a minor defect in urinary concentration because of compensation from the up‐regulated vasopressin system. However, under water restriction, SCD mice struggle to concentrate urine despite activating NFAT5. SCD‐induced urinary concentration defect appears to be resulted from the poor blood flow in vasa recta rather than the renal tubules’ ability to absorb water and solutes. SCD mice attempt to maintain normal urinary osmolality under water repletion in a vasopressin‐dependent manner. Under water restriction.
... Las complicaciones severas asociadas a la anemia falciforme involucran la expresión alterada de moléculas de adhesión y la misma deformidad de los hematíes, que desencadenan la promoción de la unión de los glóbulos rojos al endotelio [11]. Estas comprenden: hipertensión pulmonar, priapismo, enfermedad cerebrovascular, ulceración de miembros inferiores, crisis dolorosas (que hacen parte de la triada fundamental de la enfermedad que se mencionó anteriormente), dolor torácico agudo, necrosis avascular ósea, necrosis de la papila renal y anemia hemolítica severa [12,13,14]. ...
La anemia de células falciformes es la alteración hematológica heredada más común a nivel mundial. Esta dada por la presencia de hemoglobinas anormales (HbS y sus diferentes genotipos) a raíz de una mutación en las cadenas de globina. La tríada clínica consiste en eventos vaso-oclusivos, anemia hemolítica crónica y asplenia funcional. Hoy en día se ha documentado toda clase de complicaciones asociadas a la enfermedad, entre las cuales se encuentran: accidentes cerebrovasculares, infarto agudo de miocardio, hipertensión pulmonar, tromboembolismos venosos, infecciones, necrosis de la papila renal, enfermedad renal crónica, ulceraciones en miembros inferiores, enfermedades del aparato hepatobiliar y necrosis ósea avascular. Es de vital importancia la realización de un correcto enfoque clínico y terapéutico de los pacientes con anemia de células falciformes de modo que sea posible la prevención y tratamiento oportuno de las complicaciones asociadas a esta condición.
