Dengue is a viral illness spreads through the bite of Aedes aegypti mosquito leading to a serious health hazard. Dengue induced acute kidney injury is a fatal consequence and there are very few studies reported. Hence early identification of high risk groups is crucial for prevention, to restrict progression and effective treatment of acute kidney injury and to minimise associated morbidity and mortality. The coronavirus disease outbreak has widely spread into a pandemic all over the world. COVID-19 cases have presented with wide spectrum of severity ranging from a mild presentation to severe cases affecting the lungs(ARDS) mainly and rapidly affecting various body organs leading to multiorgan failure. Among these renal involvement is common, the severity of which ranges from mild loss of protein in urine to progressive acute kidney injury requiring renal replacement therapy.
Congenital abnormalities of the kidney and urinary tract (CAKUT) are a key cause of morbidity and a substantial contributor to end-stage renal disease (ESRD). These anomalies are the most prevalent form of birth malformation.Other system abnormalities such as those of the heart, gastrointestinal tract, central nervous system, skeletal system, respiratory system, facial dysmorphism, reproductive system, abdominal wall coexist with these anomalies. Congenital heart defects (CHD) are the most frequent complication in this syndrome, according to previous data. These findings show a similar genetic aetiology for congenital heart disease (CHD) and renal abnormalities, implying that CHD patients are at a significantly increased risk of renal anomaly outcomes. To avoid renal damage and chronic kidney disease, it is crucial to be aware of this linkage in the early treatment and diagnosis of CAKUT. We present a case of a 23 year old male who presented to us with symptoms of ESRD and was diagnosed to be case of CAKUT syndrome with VSD as the extra renal association.
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In this case report we discuss a patient with neurological manifestations thought to be a case of hepatic encephalopathy. With no improvement in symptoms despite treatment, it created a diagnostic dilemma. Eventually, toxicological investigations were done which revealed that heavy metal poisoning could be the possible culprit. Encephalopathy is characterised by impaired mental state as a result of a diffuse brain dysfunction or other psychiatric condition that induces unconsciousness, typically followed by diffuse electroencephalogram (EEG) anomalies. Both primary neurological and systemic disorders are root causes of encephalopathy. Encephalopathy results from several causes such as liver failure or liver cancer, metabolic abnormalities, anoxic encephalopathy, infections, exposure to harmful compounds such as lithium paint, synthetic contaminants (toxins), inflammations (systemic lupus erythematous, sarcoidosis), drug induced, demyelination (e.g., multiple sclerosis), degenerative process like Alzheimer disease, Parkinson disease and hereditary encephalopathies such as leukodystrophy of the white matter. 1 Humans have used heavy metals since many years. While many harmful health effects of heavy metals have long been established, exposure to heavy metals continues to rise in some parts of the world, especially in underdeveloped countries. Emissions have decreased over the past 100 years in most developed countries. Heavy metals are prevalent and remain in the ecosystem, in general causing bio amplification. Living systems frequently associate with heavy metals in different proportions in the habitat. Heavy metal exposure induces lipid peroxidation, Deoxyribonucleic Acid (DNA) damage and protein modification by generation of oxygen free radicals. Exposure to these metals occurs in occupational areas by equipment, air, food and drinking water. Prolonged exposure to heavy metals may lead to neurotoxicity and brain damage. When symptoms of toxic encephalopathy emerge immediately following single acute exposure to high levels of toxic chemicals it is termed as acute toxic encephalopathy. Other than that if symptoms emerge insidiously over time in association with repeated or chronic exposure to low levels of neurotoxins it is called as chronic toxic encephalopathy. 2 In some cases, diagnosis of toxic encephalopathy is complicated by the fact that toxic chemicals can also damage liver and kidneys. In these cases hepatic dysfunction must be successfully treated before diagnosis of toxic encephalopathy can be considered. It is a diagnosis of exclusion, so a full work up for other possible aetiologies such as hepatic, uremic and infectious should be done. In this case report we have discussed heavy metal encephalopathy masquerading as hepatic dysfunction.
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