BACKGROUND Acute kidney injury(AKI)due to interstitial nephritis is a known condition primarily attributed to various medications.While medication-induced interstitial nephritis is common,occurrences due to non-pharma...BACKGROUND Acute kidney injury(AKI)due to interstitial nephritis is a known condition primarily attributed to various medications.While medication-induced interstitial nephritis is common,occurrences due to non-pharmacological factors are rare.This report presents a case of severe AKI triggered by intratubular oxalate crystal deposition,leading to interstitial nephritis.The aim is to outline the case and its management,emphasizing the significance of recognizing uncommon causes of interstitial nephritis.CASE SUMMARY A 71-year-old female presented with stroke-like symptoms,including weakness,speech difficulties,and cognitive impairment.Chronic hypertension had been managed with hydrochlorothiazide(HCTZ)for over two decades.Upon admis-sion,severe hypokalemia and AKI were noted,prompting discontinuation of HCTZ and initiation of prednisolone for acute interstitial nephritis.Further investigations,including kidney biopsy,confirmed severe acute interstitial nephritis with oxalate crystal deposits as the underlying cause.Despite treatment,initial renal function showed minimal improvement.However,with prednisolone therapy and supportive measures,her condition gradually improved,high-lighting the importance of comprehensive management.CONCLUSION This case underscores the importance of a thorough diagnostic approach in identifying and addressing uncommon causes of interstitial nephritis.The occurrence of interstitial nephritis due to oxalate crystal deposition,especially without typical risk factors,emphasizes the need for vigilance in clinical practice.展开更多
BACKGROUND Arginine vasopressin is a neuropeptide produced in the hypothalamus and released by the posterior pituitary gland.In addition to maintaining plasma osmolarity,under hypovolemic or hypotensive conditions,it ...BACKGROUND Arginine vasopressin is a neuropeptide produced in the hypothalamus and released by the posterior pituitary gland.In addition to maintaining plasma osmolarity,under hypovolemic or hypotensive conditions,it helps maintain plasma volume through renal water reabsorption and increases systemic vascular tone.Its synthetic analogues are widely used in the intensive care unit as a continuous infusion,in addition to hospital floors as an intravenous or intranasal dose.A limited number of cases of hyponatremia in patients with septic or hemorrhagic shock have been reported previously with vasopressin.We report for the first time a normotensive patient who developed vasopressin-induced hyponatremia.CASE SUMMARY A 39-year-old man fell off a forklift and sustained an axial load injury to his cranium.He had no history of previous trauma.Examination was normal except for motor and sensory deficits.The Imagine test showed endplate fracture at C7 and acute traumatic disc at C7 with cortical degeneration.He underwent cervical discectomy and fusion,laminectomy,and posterior instrumented fusion.After intensive care unit admission post-surgery,he developed hyponatremia of 121-124 mEq/L post phenylephrine and vasopressin infusion to maintain blood pressure maintenance.He was evaluated for syndrome of inappropriate secretion of antidiuretic hormone,hypothyroid,adrenal-induced,or diuretic-induced hyponatremia.At the end of extensive evaluation for the underlying cause of hyponatremia,vasopressin was discontinued.He was also put on fluid restriction,given exogenous desmopressin,and a dextrose 5%in water infusion to prevent osmotic demyelination syndrome caused by sodium overcorrection which improved his sodium level to 135 mmol/L.CONCLUSION The presentation of vasopressin-induced hyponatremia is uncommon in normotensive patients,and the most difficult aspect of this condition is determining the underlying cause of hyponatremia.Our case illustrates that,considering the vast differential diagnosis of hyponatremia in hospitalized patients,both hospitalists and intensivists should be aware of this serious complication of vasopressin therapy.展开更多
BACKGROUND Diabetic ketoacidosis(DKA)and hyperglycemic hyperosmolar state(HHS)are common acute complications of diabetes mellitus with a high risk of mortality.When combined with hypernatremia,the complications can be...BACKGROUND Diabetic ketoacidosis(DKA)and hyperglycemic hyperosmolar state(HHS)are common acute complications of diabetes mellitus with a high risk of mortality.When combined with hypernatremia,the complications can be even worse.Hypernatremia is a rarely associated with DKA and HHS as both are usually accompanied by normal sodium or hyponatremia.As a result,a structured and systematic treatment approach is critical.We discuss the therapeutic approach and implications of this uncommon presentation.CASE SUMMARY A 62-year-old man with no known past medical history presented to emergency department with altered mental status.Initial work up in emergency room showed severe hyperglycemia with a glucose level of 1093 mg/dL and severe hypernatremia with a serum sodium level of 169 mEq/L.He was admitted to the intensive care unit(ICU)and was started on insulin drip as per DKA protocol.Within 12 h of ICU admission,blood sugar was 300 mg/dL.But his mental status didn’t show much improvement.He was dehydrated and had a corrected serum sodium level of>190 mEq/L.As a result,dextrose 5%in water and ringer's lactate were started.He was also given free water via an nasogastric(NG)tube and IV Desmopressin to improve his free water deficit,which improved his serum sodium to 140 mEq/L.CONCLUSION The combination of DKA,HHS and hypernatremia is rare and extremely challenging to manage,but the most challenging part of this condition is selecting the correct type of fluids to treat these conditions.Our case illustrates that desmopressin and free water administration via the NG route can be helpful in this situation.展开更多
BACKGROUND Anaplasmosis is a tick-borne disease with a range of clinical manifestations,from a flu-like illness with fever and myalgias to a severe systemic disease with multisystem organ failure.Although renal involv...BACKGROUND Anaplasmosis is a tick-borne disease with a range of clinical manifestations,from a flu-like illness with fever and myalgias to a severe systemic disease with multisystem organ failure.Although renal involvement is not a common presentation,there have been few cases reporting acute kidney injury from Anaplasmosis.CASE SUMMARY We present a 55-year-old female with anaplasmosis who developed acute kidney injury due to membranoproliferative glomerulonephritis(MPGN).The patient originally presented with cough and shortness of breath.She was admitted to the hospital with a diagnosis of community acquired pneumonia and received antibiotics.During the hospital course she developed severe acute renal failure.Initial serological work up didn’t provide any conclusive diagnosis.Hence,she underwent kidney biopsy which showed MPGN pattern suggesting autoimmune,multiple myeloma or infectious etiology.Extensive work up was undertaken which was negative for autoimmune diseases,vasculitis panel,paraproteinemias but tested positive for IgG anaplasma with high titers indicating Anaplasmosis.CONCLUSION Our case shows a unique presentation of severe acute renal failure from MPGN from tick borne illness.MPGN is usually seen with autoimmune diseases,hepatitis C virus infections,paraproteinemias.Hence,we suggest that tick borne illness should also be considered when evaluating acute renal failure cases in tick borne prevalent regions.展开更多
文摘BACKGROUND Acute kidney injury(AKI)due to interstitial nephritis is a known condition primarily attributed to various medications.While medication-induced interstitial nephritis is common,occurrences due to non-pharmacological factors are rare.This report presents a case of severe AKI triggered by intratubular oxalate crystal deposition,leading to interstitial nephritis.The aim is to outline the case and its management,emphasizing the significance of recognizing uncommon causes of interstitial nephritis.CASE SUMMARY A 71-year-old female presented with stroke-like symptoms,including weakness,speech difficulties,and cognitive impairment.Chronic hypertension had been managed with hydrochlorothiazide(HCTZ)for over two decades.Upon admis-sion,severe hypokalemia and AKI were noted,prompting discontinuation of HCTZ and initiation of prednisolone for acute interstitial nephritis.Further investigations,including kidney biopsy,confirmed severe acute interstitial nephritis with oxalate crystal deposits as the underlying cause.Despite treatment,initial renal function showed minimal improvement.However,with prednisolone therapy and supportive measures,her condition gradually improved,high-lighting the importance of comprehensive management.CONCLUSION This case underscores the importance of a thorough diagnostic approach in identifying and addressing uncommon causes of interstitial nephritis.The occurrence of interstitial nephritis due to oxalate crystal deposition,especially without typical risk factors,emphasizes the need for vigilance in clinical practice.
文摘BACKGROUND Arginine vasopressin is a neuropeptide produced in the hypothalamus and released by the posterior pituitary gland.In addition to maintaining plasma osmolarity,under hypovolemic or hypotensive conditions,it helps maintain plasma volume through renal water reabsorption and increases systemic vascular tone.Its synthetic analogues are widely used in the intensive care unit as a continuous infusion,in addition to hospital floors as an intravenous or intranasal dose.A limited number of cases of hyponatremia in patients with septic or hemorrhagic shock have been reported previously with vasopressin.We report for the first time a normotensive patient who developed vasopressin-induced hyponatremia.CASE SUMMARY A 39-year-old man fell off a forklift and sustained an axial load injury to his cranium.He had no history of previous trauma.Examination was normal except for motor and sensory deficits.The Imagine test showed endplate fracture at C7 and acute traumatic disc at C7 with cortical degeneration.He underwent cervical discectomy and fusion,laminectomy,and posterior instrumented fusion.After intensive care unit admission post-surgery,he developed hyponatremia of 121-124 mEq/L post phenylephrine and vasopressin infusion to maintain blood pressure maintenance.He was evaluated for syndrome of inappropriate secretion of antidiuretic hormone,hypothyroid,adrenal-induced,or diuretic-induced hyponatremia.At the end of extensive evaluation for the underlying cause of hyponatremia,vasopressin was discontinued.He was also put on fluid restriction,given exogenous desmopressin,and a dextrose 5%in water infusion to prevent osmotic demyelination syndrome caused by sodium overcorrection which improved his sodium level to 135 mmol/L.CONCLUSION The presentation of vasopressin-induced hyponatremia is uncommon in normotensive patients,and the most difficult aspect of this condition is determining the underlying cause of hyponatremia.Our case illustrates that,considering the vast differential diagnosis of hyponatremia in hospitalized patients,both hospitalists and intensivists should be aware of this serious complication of vasopressin therapy.
文摘BACKGROUND Diabetic ketoacidosis(DKA)and hyperglycemic hyperosmolar state(HHS)are common acute complications of diabetes mellitus with a high risk of mortality.When combined with hypernatremia,the complications can be even worse.Hypernatremia is a rarely associated with DKA and HHS as both are usually accompanied by normal sodium or hyponatremia.As a result,a structured and systematic treatment approach is critical.We discuss the therapeutic approach and implications of this uncommon presentation.CASE SUMMARY A 62-year-old man with no known past medical history presented to emergency department with altered mental status.Initial work up in emergency room showed severe hyperglycemia with a glucose level of 1093 mg/dL and severe hypernatremia with a serum sodium level of 169 mEq/L.He was admitted to the intensive care unit(ICU)and was started on insulin drip as per DKA protocol.Within 12 h of ICU admission,blood sugar was 300 mg/dL.But his mental status didn’t show much improvement.He was dehydrated and had a corrected serum sodium level of>190 mEq/L.As a result,dextrose 5%in water and ringer's lactate were started.He was also given free water via an nasogastric(NG)tube and IV Desmopressin to improve his free water deficit,which improved his serum sodium to 140 mEq/L.CONCLUSION The combination of DKA,HHS and hypernatremia is rare and extremely challenging to manage,but the most challenging part of this condition is selecting the correct type of fluids to treat these conditions.Our case illustrates that desmopressin and free water administration via the NG route can be helpful in this situation.
文摘BACKGROUND Anaplasmosis is a tick-borne disease with a range of clinical manifestations,from a flu-like illness with fever and myalgias to a severe systemic disease with multisystem organ failure.Although renal involvement is not a common presentation,there have been few cases reporting acute kidney injury from Anaplasmosis.CASE SUMMARY We present a 55-year-old female with anaplasmosis who developed acute kidney injury due to membranoproliferative glomerulonephritis(MPGN).The patient originally presented with cough and shortness of breath.She was admitted to the hospital with a diagnosis of community acquired pneumonia and received antibiotics.During the hospital course she developed severe acute renal failure.Initial serological work up didn’t provide any conclusive diagnosis.Hence,she underwent kidney biopsy which showed MPGN pattern suggesting autoimmune,multiple myeloma or infectious etiology.Extensive work up was undertaken which was negative for autoimmune diseases,vasculitis panel,paraproteinemias but tested positive for IgG anaplasma with high titers indicating Anaplasmosis.CONCLUSION Our case shows a unique presentation of severe acute renal failure from MPGN from tick borne illness.MPGN is usually seen with autoimmune diseases,hepatitis C virus infections,paraproteinemias.Hence,we suggest that tick borne illness should also be considered when evaluating acute renal failure cases in tick borne prevalent regions.
