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RenalInsufficiency

Category

788d8fc5f5f164e2bf398ac9335ba880d41c55937757967738710806
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5717

Acute Renal Failure Explained Clearly

Understand acute renal failure (also called acute kidney injury) with this clear explanation from Dr. Seheult. This is video 1 of 3 on acute renal failure.  
YouTube
over 5 years ago
Preview
21
600

Acute Kidney Injury

A quick presentation on Acute Kidney Injury in enough depth for an F1/F2.  
Hamed N.H.Gilani
over 8 years ago
7
13
291

Acute Renal Failure

Acute renal failure is a dreaded complication in the ICU.  This podcast will review the various types of acute renal failure, the etiology, as well as acute management.  
Jeffrey S. Guy, MD, FACS
about 9 years ago
9
11
674

Intro to Renal Failure

Positive urine sediment and/or RBCs should always point you to intrinsic renal failure (ATN, AIN, glomerulonephritis), regardless of urine sodium and osmolal...  
youtube.com
almost 4 years ago
Preview
8
176

Acute Renal Failure Explained Clearly

Understand Acute Renal Failure (also called acute kidney injury) with this clear explanation from Dr. Seheult.  
YouTube
over 5 years ago
Preview
7
213

Complications of High Blood Pressure or Hypertension - adidarwinian

Complications of High Blood Pressure or Hypertension can be a multitude of deadly diseases including Heart Attack, Stroke, Kidney Failure, Vision Loss, etc.  
adidarwinian.com
almost 5 years ago
Preview
6
863

Chronic Kidney Disease | Clinical Gate

The kidney is one of the most highly differentiated organs in the body. At the conclusion of embryologic development, nearly 30 different cell types form a multitude of filtering capillaries and segmented nephrons enveloped by a dynamic interstitium. This cellular diversity modulates a variety of complex physiologic processes. Endocrine functions, the regulation of blood pressure and intraglomerular hemodynamics, solute and water transport, acid-base balance, and removal of drug metabolites are all accomplished by intricate mechanisms of renal response. This breadth of physiology hinges on the clever ingenuity of nephron architecture that evolved as complex organisms came out of water to live on land.  
clinicalgate.com
almost 4 years ago
Preview
4
97

Advanced cervical cancer and renal failure

A presentation for palliative care and oncology  
James Harper
almost 11 years ago
Foo20151013 2023 2njk5o?1444774020
4
1326

LWW: Case Of The Month - April 2013

This month’s case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e, with 15% off using the discount code: MEDUCATION. The case below is followed by a quiz question, allowing you a choice of diagnoses. Select the one letter section that best describes the patient’s condition. The Case A 28-year old woman has an unremarkable pregnancy through her first 28 weeks of gestation, with normal weight gain and no serious complications. She has no previous history of diabetes, hypertension of other systemic disease before or during her current pregnancy. During her 30-week checkup, her blood pressure measures 128/85, and she complains about feeling slightly more “bloated” than usual with swelling in her legs that seems to get more uncomfortable as the day goes on. Her obsterician recommends that she get more bed rest, stay off her feet as much as possible and return for evaluation in one week. At the one-week follow-up, the patient presents with noticable”puffiness” in her face, and a blood pressure of 145/95. She complains she has been developing headaches, sporadic blurred vision, right-sided discomfort and some shortness of breath. She has gained more than 10 lb (4.5kg) in the past week. A urinalysis on the patient revelas no glucose but a 3+ reading for protein. Her obstetrician decides to admit her immediately to a local tertiary care hospital for further evaluation. Over the next 24 hours, the patient’s urine output is recorded as 500mL and contains 6.8 grams of protein. Her plasma albumin level is 3.1 g/dl, hemacrit 48%, indirect bilirubin 1.5mg/dl and blood platelets=77000/uL, respectively. Her blood pressure is now 190/100. It is decided to try to deliver the foetus. The expelled placenta is small and shows signs of widespread ischmic damage. Within a week of delivery, the mother’s blood pressure returns to normal, and her oedema subsides. One month later, the mother shows no ill effects of thos later-term syndrome. Question What is the clinical diagnosis of this patient’s condition and its underlying pathophysiology? A. Gestational Hypertension B. Preeclampsia C. Gestational Diabetes D. Compression of the Inferior Vena Cava Answer The correct answer is "B. Preeclampsia". The patient’s symptoms and laboratory findings are consistent with a diagnosis of Preeclampsia, which is a condition occurring in some pregnancies that causes life-threatening organ and whole body regulatory malfunctions. The patient’s negative urine glucose is inconsistent with gestational diabetes. Gestational hypertension or vena caval compression cannot explain all of the patient findings. The patient has three major abnormal findings- generalised oedema, hypertension and proteinuria which are all common in preeclampsia. Although sequalae of a normal pregnancy can include water and salt retention, bloating, modest hypertension and leg swelling (secondary to capillary fluid loss from increased lower limb capillary hydrostatic pressure due to compression of the inferior vena cava by the growing foetus/uterus), oedema in the head and upper extremities, a rapid 10 pound weight gain and shortness of breath suggests a generalized and serious oedematous state. The patient did not have hypertension before or within 20 weeks gestation (primary hypertension) and did not develop hypertension after the 20th week of pregnancy with no other abnormal findings (gestational hypertension). Hypertension with proteinuria occurring beyond the 20th week of pregnancy however is a hallmark of preeclampsia. In addition, the patient has hemolysis (elevated bilirubin and LDH levels), elevated liver enzyme levels and thrombocytopenia. This is called the HELLP syndrome (HELLP = Hemolysis, Elevated Liver enzymes and Low Platelets.), and is considered evidence of serious patient deterioration in preeclampsia. A urine output of 500 ml in 24 hours is 1/2 to 1/4 of normal output in a hydrated female and indicates renal insufficiency. Protein should never be found in the urine and indicates loss of capillaries integrity in glomeruli which normally are not permeable to proteins. The patient has substantial 24 urine protein loss and hypoalbuminemia. However, generally plasma albumin levels must drop below 2.5 gm/dl to decrease plasma oncotic pressure enough to cause general oedema. The patient’s total urinary protein loss was insufficient in this regard. Capillary hyperpermeability occurs with preeclampsia and, along with hypertension, could facilitate capillary water efflux and generalized oedema. However myogenic constriction of pre-capillary arterioles could reduce the effect of high blood pressure on capillary water efflux. An early increase in hematocrit in this patient suggests hemoconcentration which could be caused by capillary fluid loss but the patient’s value of 48 is unremarkable and of little diagnostic value because increased hematocrit occurs in both preeclampsia and normal pregnancy. PGI2, PGE2 and NO, produced during normal pregnancy, cause vasorelaxation and luminal expansion of uterine arteries, which supports placental blood flow and development. Current theory suggests that over production of endothelin, thromboxane and oxygen radicals in preeclampsia antagonize vasorelaxation while stimulating platelet aggregation, microthrombi formation and endothelial destruction. These could cause oedema, hypertension, renal/hepatic deterioration and placental ischemia with release of vasotoxic factors. The patient’s right-sided pain is consistent with liver pathology (secondary to hepatic DIC or oedematous distention). Severe hypertension in preeclampsia can lead to maternal end organ damage, stroke, and death. Oedematous distension of the liver can cause hepatic rupture and internal hemorrhagic shock. Having this patient carry the baby to term markedly risks the life of the mother and is not considered current acceptable clinical practice. Delivery of the foetus and termination of the pregnancy is the only certain way to end preeclampsia. Read more This case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e. Save 15% (and get free P&P) on this, and a whole host of other LWW titles at (lww.co.uk)[http://lww.co.uk] when you use the code MEDUCATION when you check out! About LWW/ Wolters Kluwer Health Lippincott Williams and Wilkins (LWW) is a leading publisher of high-quality content for students and practitioners in medical and related fields. Their text and review products, eBooks, mobile apps and online solutions support students, educators, and instiutions throughout the professional’s career. LWW are proud to partner with Meducation.  
Lippincott Williams & Wilkins
over 6 years ago
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4
116

Prerenal Acute Renal Failure with High FENa (Fractional Excretion of Sodium)

Very good case in showing a frequently overlooked issue of diuretics. Remember, there is almost never a reason to give both fluids and diuretics...make up your mind. IV fluids are the #1 method to try in oliguric pts NOT Lasix.Do not agree with Foley cath placement if patient is able to urinate and can check creatinine to know pt is improving. Any catheter is a foreign body and increases infection risk.It is also very uncomfortable for patients.Not sure why U/S of kidney needed right away either unless the patient has chronic kidney disease or does not improve with fluids.Unnecessary tests add to the expense of healthcare which all of us pay for. This increases insurance costs, medicaid costs, etc so much it can put companies (and gov't in the future?) out of business.  
clinicalcases.org
about 4 years ago
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4
11

Incidence and Outcomes in Acute Kidney Injury: A Comprehensive Population-Based Study

Epidemiological studies of acute kidney injury (AKI) and acute-on-chronic renal failure (ACRF) are surprisingly sparse and confounded by differences in definition. Reported incidences vary, with few studies being population-based. Given this and our aging population, the incidence of AKI may be much higher than currently thought. We tested the hypothesis that the incidence is higher by including all patients with AKI (in a geographical population base of 523,390) regardless of whether they required renal replacement therapy irrespective of the hospital setting in which they were treated. We also tested the hypothesis that the Risk, Injury, Failure, Loss, and End-Stage Kidney (RIFLE) classification predicts outcomes. We identified all patients with serum creatinine concentrations ≥150 μmol/L (male) or ≥130μmol/L (female) over a 6-mo period in 2003. Clinical outcomes were obtained from each patient's case records. The incidences of AKI and ACRF were 1811 and 336 per million population, respectively. Median age was 76 yr for AKI and 80.5 yr for ACRF. Sepsis was a precipitating factor in 47% of patients. The RIFLE classification was useful for predicting full recovery of renal function (P < 0.001), renal replacement therapy requirement (P < 0.001), length of hospital stay [excluding those who died during admission (P < 0.001)], and in-hospital mortality (P = 0.035). RIFLE did not predict mortality at 90 d or 6 mo. Thus the incidence of AKI is much higher than previously thought, with implications for service planning and providing information to colleagues about methods to prevent deterioration of renal function. The RIFLE classification is useful for identifying patients at greatest risk of adverse short-term outcomes.  
jasn.asnjournals.org
about 4 years ago
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4
245

How Diabetes and Hypertension Can Lead To CKD

Hypertension (i.e. high blood pressure) and Diabetes are two of the most common causes of kidney failure in North America. These conditions can cause irreversible damage to the kidneys over a long period of time, leading to what is known as Chronic Kidney Disease (CKD).  
youtube.com
almost 4 years ago
30095
3
108

Acute Renal Failure

Video tutorial on acute renal failure outlining the definition, important causes, presentation and basic management.  
Podmedics
almost 8 years ago
30096
3
217

The Basics of Renal failure

Video tutorial on the basics of renal failure.  
Podmedics
almost 8 years ago
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2
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CDC will explore kidney failure epidemic among agricultural workers

The US Centers for Disease Control and Prevention (CDC) has launched three new studies to examine a lethal epidemic of kidney failure that has killed agricultural workers along Central America’s Pacific coast and in regions of Sri Lanka, India, and Egypt.  
bmj.com
over 5 years ago
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2
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Acute Renal Failure

https://www.facebook.com/ArmandoHasudungan Support me: http://www.patreon.com/armando Instagram: http://instagram.com/armandohasudungan Twitter: https://twit...  
YouTube
over 4 years ago
Preview
2
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Clinical Cases and Images: ClinicalCases.org: Prerenal Acute Renal Failure due to Volume Depletion

This is a good practical case and very useful for new clinicians. For any clinician:No foley catheter unless oliguric, anuric, obstructed since any catheter is a foreign body and increases infection risk.Rehydrate if U/A has high spec gavity, mucous membranes dry, or if BUN is >30 times the creatinine as in this case. Even CHF pts get dry if not in heart failure. If in doubt, do CXR, BNPT, listen for crackles.Start with 250cc IVF if BNPT not less than 150 or give carefully while checking lung bases posteriorly after each bolus along with pulse ox, etc as above. Half of pts in acute renal failure are septic. Look for and eliminate source such as pneumonia, foreign body, pyelonephritis, joint infections. May be afebrile/ low temp or low WBCs with sepsis. Do cultures, check lactate ASAP to detect sepsis BEFORE the BP drops. Lactic acid "the troponin of sepsis." If septic, give a lot of fluids (up to 10 liters often) since capillary leak syndrome will lead to severe hypotension. If septic expect edema to develop with IV boluses yet be aware pt is intravascularly depleted. No pressors without fluids "pressors are not your friend" as per lecturers on Surviving Sepsis campaign.  
clinicalcases.org
about 4 years ago
10
1
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Crush Syndrome

<p>Earthquakes are horrible natural events causing loss of lives in the thousands.&nbsp;&nbsp; Following earthquakes, building collapses, and cave-ins, large number of victims will suffer from renal failure and death following crush syndrome.&nbsp; </p>  
Jeffrey S. Guy, MD, FACS
about 9 years ago
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1
14

A case of renal failure

Medical Protection Society Website  
medicalprotection.org
over 5 years ago