Clinical, Etiological and Progressive Aspects of Acute Tubular Necrosis of Toxic Origin at the Brazzaville University Hospital Center

Background and Objectives: Acute tubular necrosis (ATN) is the second cause of acute kidney injury (AKI) in an intra-hospital environment. The toxic origin is avoidable. Our objectives were to determine the toxic substances at the origin of ATN at the Brazzaville University Hospital and determine the evolving aspects and the factors associated with it. Patients and Methods: We carried out a 12-month from June 20, 2022 to June 30, 2023. It was a prospective observational study in the Nephrology Department of Brazzaville University Hospital Center. The diagnosis of ATN was done in the presence of AKI occurring in the context of taking nephrotoxic substances with negative albuminuria. Cases of ATN aggravating CKD were excluded. Data analysis was done with Epi-Info 7.2 software. Results: We identified 63 cases of AKI on toxic ATN. Their average age was 47 ± 19 years with a male predominance of 60.2%. The 3 main toxicants incriminated were: herbal medicine (49.2%), Gentamycin (17.5%) and non-steroidal anti-inflammatory drugs (14.3%). An indication for hemodialysis was made in 43 patients (68.2%), the evolution was marked by a cure in 29 patients (46.1%), 10 (15.9%) became chronic kidney failure, 19 (30.1%) died, 5 (7.9%) were lost to follow-up. The main factor for non-healing is anuria (p Conclusion: The main cause of toxic ATN at Brazzaville University Hospital is herbal medicine. The death rate is high there.

Approach to Acute Kidney Injury: Diagnosis and Management

Acute kidney injury is a critical but commonly occurring medical condition that presents with a sudden decline in kidney function. This comprehensive review article provides an in-depth examination of the risk elements, etiology, diagnosis, management, and preventive approach of AKI. The causes that contribute to the development of AKI include prerenal, intrinsic renal, and postrenal. The diagnostic approach to AKI includes clinical, laboratory, and imaging studies to evaluate the root cause analysis and to find out the severity of kidney injury. Timely and accurate diagnosis is crucial for initiating appropriate management strategies. The treatment strategies may include fluid and electrolyte management, medication adjustments, nutritional support, and renal replacement therapy. The prospect of recovery diverges as it relies on the individual factors, reasons, and gravity of the condition. This review highlights the importance of raising awareness among healthcare professionals and the public about AKI, early recognition of risk factors, and prompt management. Further research is needed to explore novel therapeutic approaches and refine existing management guidelines for this critical condition.

Nephropathy in dietary hyperoxaluria:A potentially preventable acute or chronic kidney disease

Hyperoxaluria can cause not only nephrolithiasis and nephrocalcinosis,but also renal parenchymal disease histologically characterized by deposition of calcium oxalate crystals throughout the renal parenchyma,profound tubular damage and interstitial inflammation and fibrosis.Hyperoxaluric nephropathy presents clinically as acute or chronic renal failure that may progress to endstage renal disease(ESRD).This sequence of events,well recognized in the past in primary and enteric hyperoxalurias,has also been documented in a few cases of dietary hyperoxaluria.Estimates of oxalate intake in patients with chronic dietary hyperoxaluria who developed chronic kidney disease or ESRD were comparable to the reported average oxalate content of the diets of certain populations worldwide,thus raising the question whether dietary hyperoxaluria is a primary cause of ESRD in these regions.Studies addressing this question have the potential of improving population health and should be undertaken,alongside ongoing studies which are yielding fresh insights into the mechanisms of intestinal absorption and renal excretion of oxalate,and into the mechanisms of development of oxalate-induced renal parenchymal disease.Novel preventive and therapeutic strategies for treating all types of hyperoxaluria are expected to develop from these studies.

Acute Kidney Injury (AKI) in the Setting of Multi-Organ Dysfunction Syndrome (MODS) Secondary to Yellow Fever Infection (YFI) in a 19-Year-Old Woman

Background: Outbreak of yellow fever infection (YFI), a mosquito-borne disease, occurs sporadically worldwide especially in tropical nations. Acute kidney injury (AKI) commonly results from YFI and could be associated with a poor prognosis for victims even under intensive care unit (ICU). Pathophysiologic mechanisms for AKI include hypovolemic shut down, cytotoxicity, acute tubular necrosis (ATN), hemolysis, or coagulopathy. Early diagnosis, prompt and effective treatment modalities including dialysis improve treatment outcome. Aim: We report the case management of a 19-year-old woman who had yellow fever infection complicated by acute kidney injury in the setting of multi-organ dysfunction syndrome (MODS). Case Presentation: A 19-year-old woman who presented with fever, headache and vomiting for 2 weeks. In the course of the illness, urine volume became reduced and coke colored, followed by body swelling, yellowness of the eyes bleeding from the orifices. Examination revealed an acutely ill looking woman, icteric, and with pedal edema. Her pulse was 100/min and blood pressure was 120/80 mmHg. Liver was enlarged, soft and tender. She had proteinuria 3+ and polymerase chain reaction (PCR) confirmed yellow fever infection. She had markedly deranged serum biochemical parameters for which she had a three-hour session of hemodialysis with Heparin anticoagulation. The urea reduction ratio (URR) was 46.9%. Barrier nursing was commenced. She had 7 units of whole blood and a pint of fresh frozen plasma (FFP) with antibiotics, Rabeprazole, Tranexamic acid, Vitamin K and Frusemide. She had the second dialysis session of HD and entered into the recovering phase of AKI and was subsequently discharged after 18th days on admission. Conclusion: Yellow fever infection occurs sporadically and could lead to MODS involving the kidneys, liver and hematologic system. Prompt initiation of dialysis, correction of coagulopathy, and antibiotics use are measures needed to arrest progression and death. Vaccination, destruction of the natural habitat of the carrier and infective organisms are necessary particularly in endemic regions of the world.

Clinicopathological spectrum of snake bite-induced acute kidney injury from India

AIM To study the clinico-pathological spectrum of snake bite-induced acute kidney injury(AKI).METHODS A retrospective study of patients admitted at Indira Gandhi Medical College Hospital,Shimla with snake bite-induced AKI from July 2003 to June 2016.Medical records were evaluated for patient's information on demographic,clinical characteristics,complications and outcome.Outcomes of duration of hospital stay,requirement for intensive care unit support,treatment with dialysis,survival and mortality were analyzed.The survival and non survival groups were compared to see the difference in the demographic factors,clinical characteristics,laboratory results,and complications.In patients subjected to kidney biopsy,the findings of histopathological examination of the kidney biopsies were also analyzed.RESULTS One hundred and twenty-one patients were diagnosed with snake bite-induced AKI.Mean age was 42.2 ± 15.1 years and majority(58%) were women.Clinical details were available in 88 patients.The mean duration of arrival at hospital was 3.4 ± 3.7 d with a range of 1 to30 d.Eighty percent had oliguria and 55% had history of having passed red or brown colored urine.Coagulation defect was seen in 89% patients.The hematological and biochemical laboratory abnormalities were:Anemia(80.7%),leukocytosis(75%),thrombocytopenia(47.7%),hyperkalemia(25%),severe metabolic acidosis(39.8%),hepatic dysfunction(40.9%),hemolysis(85.2%) and rhabdomyolysis(68.2%).Main complications were:Gastrointestinal bleed(12.5%),seizure/encephalopathy(10.2%),hypertension,pneumonia/acute respiratory distress syndrome(ARDS) and disseminated intravascular coagulation(9.1% each),hypotension and multi organ failure(MOF)(4.5% each).Eighty-two percent patients required renal replacement therapy.One hundred and ten(90.9%) patient survived and 11(9.1%) patients died.As compared to the survival group,the white blood cell count(P = 0.023) and bilirubin levels(P = 0.006) were significant higher and albumin levels were significantly lower(0.005) in patients who died.The proportion of patients with pneumonia/ARDS(P = 0.001),seizure/encephalopathy(P = 0.005),MOF(P = 0.05) and need for intensive care unit support(0.001) was significantly higher and duration of hospital stay was significantly shorter(P = 0.012) in patients who died.Kidney biopsy was done in total of 22 patients.Predominant lesion on kidney biopsy was acute tubular necrosis(ATN) in 20(91%) cases.In 11 cases had severe ATN and in other nine(41%) cases kidney biopsy showed features of ATN associated with mild to moderate acute interstitial nephritis(AIN).One patient only had moderate AIN and one had patchy renal cortical necrosis(RCN).CONCLUSION AKI due to snake bite is severe and a high proportion requires renal replacement therapy.On renal histology ATN and AIN are common,RCN is rare.