Special Consideration on Fluid and Electrolytes in Acute Kidney Injury and Kidney Transplantation. AR is an 1. 1 year old African American female who was previously healthy until few months prior to the presentation at a local emergency room ER. She had anorexia, sleepiness, body weakness, and close to 1. She had an increased frequency of emesis in the last few weeks, and an associated diarrhea for 3 days. Her current medications included apple cider vinegar and an unidentified enzyme supplement both of which were obtained from a health food store for symptomatic relief. Her perinatal history was uneventful and immunization was up to date. What in the history suggests a possible diagnosis of kidney injury The history highlights a common clinical scenario in the presentation of chronic kidney disease. This girl had been sick for a minimum of 5 months. She presented with protracted uremic symptoms but apparently because of an adequate renal reserve visit to the ER was avoided until the later phase of the illness. Uremia alters the control of hungersatiety cycle by increasing brain secretion of anorectic serotonin, and causing a decreased synthesis of appetite stimulant neuropeptide Y. In addition to low caloric intake, catabolism with weight loss is promoted by pro inflammatory cytokines IL 1, elaboration of leptin, and metabolic acidosis. Anemia and metabolic acidosis are contributory to body weakness and somnolence. The protracted symptoms, in the setting of a poor accessibility to health care services, may promote risky behavior such as seeking homeopathic medicine or over the counter therapy. Often, these non FDA approved alternative agents largely untested for nephrotoxicity may cause further kidney injury. Medication such as nonsteroidal anti inflammatory drug may also cause a rapid loss in renal function leading to deterioration in a compensated kidney disease. Her symptoms progressively worsen over the months, and in the last 1 week an acute deterioration necessitates urgent medical services. What are the common chronic kidney diseases in which family history could be helpful in making diagnosis Common kidney diseases with strong family history are Alport nephritis X linked or autosomal inheritance, polycystic kidney disease autosomal recessive or dominant, and nephrogenic diabetes insipidus X linked or autosomal. Focal segmental glomerulosclerosis FSGS is a common cause of nephrotic syndrome particularly in African American population. FSGS is heterogeneous kidney disease, some of which have clearly defined genetic mutation that involves functional integrity of podocytes a component of foot process in the glomerulus important for ultrafiltration. The family history in this patient is highly suspicious of a possible diagnosis of FSGS. Both parents and a maternal aunt were on dialysis for end stage kidney disease. Except for the maternal aunt who had a preceding nephrotic syndrome the etiology of end stage kidney disease was unknown in both parents. Candidates who have passed two years P. U. C. examination of Karnataka P. Sixth Edition, 2003, ELBS. A. Quality control of herbal drugs, 1st ed. Business. FN Beverages Marketing Sdn Bhd and FN Beverages Manufacturing Sdn Bhd, collectively, FN Beverages, form the soft drinks division of Fraser Neave Holdings Bhd. F. Abnormalities in water homeostasis, as manifested by low or high serum sodium, are a commonly encountered electrolyte disorder especially in hospitalized patients. Office Small Business Edition 2003 Isotonic MuscleHer paternal grandmother died of chronic kidney disease. Her 2. 0 year old brother and 1. Review of the system was unremarkable. If this is an acute on chronic kidney injury, what are the expected physical findings Protracted fluid loss might have resulted in dehydration. On the other hand, long standing oliguria may predispose to fluid retention including body edema, congestive heart failure CHF, and pulmonary edema. Severe hypertension with or without encephalopathy is a likely complication. Advanced kidney disease may present with anemia because of erythropoietin deficiency or dilutional effect of fluid retention. Deficient 1 alpha hydroxylation of 2. D and secondary hyperparathyroidism may result in hypocalcemia. Impaired glomerular filtration reduces renal phosphate clearance. Metabolic acidosis may lead to lethargy and acidotic hyperventilation. Hyperkalemia is a possible complication due to impaired potassium clearance and an extracellular shift of potassium in exchange for hydrogen ions. On the other hand, she may also have hypokalemia because of the protracted emesis and total body potassium depletion from skeletal muscle wasting. Her clinical and laboratory findings reflect a number of the projected possibilities she had a normal mental status, good nutritional status, moderate pallor, mildmoderate dehydration, but there was no jaundice, body edema, or peripheral adenopathy. Her axillary temperature was 9. F, pulse rate 7. 5min, RR 2. BP 1. 621. 771. Hg, and pulse oximetry was 9. Her height was 1. Other physical findings were not clinically significant. Laboratory analysis WBC was 5. L, hematocrit 2. 2. Serum Na was 1. 37 m. EqL, K 2. 6 m. EqL, Cl 9. EqL, HCO3 1. 9 m. EqL, glucose 7. 7 mgd. L, BUN 9. 3 mgd. L, Cr 1. 8. 7 mgd. L, Ca 4. 3 mgd. L, P 9. L, and albumin 4. L. Urine had a p. H of 6. 5, protein was 3. L, was positive for ketones, but glucose was negative. EKG showed a prolonged QTc interval with no arrhythmia. Echocardiogram showed a mild decrease in ventricular contractility. Her calculated GFR c. GFR by Schwartz formula isbeginarrayl rmc. GFR k times rm Ht, cmSerum, Cr, mgd. L 0rm. 5. GFR e. GFR rm c. GFRe. GFR times rm 1. GFR estimated normal GFR for ageUsing the p. RIFLE criteria see Table 1, she has a stage 3 AKI or acute kidney failure AKF. Thus, most likely she has an acute loss in GFR on a pre existing kidney injury. Because there is hardly any chance for renal recovery, a chronic maintenance dialysis will be ultimately required. Note that she presented with a weight of 4. With the loss of 1. Using the baseline weight to calculate her body mass index BMI, the value equals 2. Thus obesity is a contributing factor to the kidney failure. The ensuing weight loss in the course of her illness is an adaptive mechanism by the kidney to minimize the metabolic load of obesity. This is one of the reasons why kidney may be so resilient, and why kidney injury may last long before obvious clinical manifestation. What are the immediate and long term therapeutic concerns Life threatening complications must be addressed immediately including cardiac toxicity prolonged QTc from hypocalcemia andor hypokalemia and correction of fluid deficiency. Infusion of bicarbonate was not a priority because of its less severe deficit and due to the danger of hypocalcemic tetany. Blood transfusion may be avoided if there are no symptoms attributed to anemia. Otherwise, it may be given during dialysis to avoid fluid overload in the presence of oliguric kidney injury. Severe hypertension should be reduced slowly 5. If there is hypertensive encephalopathy, immediate intravenous therapy with nicardipine, labetalol, diazoxide, or sodium nitroprusside is administered. After the initial hemodynamic stability, central dialysis catheter is inserted and acute hemodialysis is provided. To maintain fluid and electrolyte homeostasis, and restore important renal function deficit, chronic dialysis is offered while supportive care is instituted for anemia, Vitamin D deficiency, hyperphosphatemia, hypertension, and nutritional deficit. Dialysis modality is not an end in itself but a transitional procedure that will allow for eventual renal allograft transplantation. Acute therapy for the patient included infusion of 5 dextrose and half saline with 2. EqL per liter of potassium chloride to correct dehydration and hypokalemia, intravenous Ca gluconate for severe hypocalcemia restoring EKG changes back to normal, and thereafter acute hemodialysis. Chronic supportive care included home peritoneal dialysis, sevelamer hydrochloride as phosphate binder, erythropoietin for anemia, nifedipine for hypertension, and 1, 2. Vitamin D as maintenance therapy for Ca deficiency. After an extensive pre transplant work up, she was placed on a waiting list for cadaveric transplantation. Ten months after the initial diagnosis, she was offered the kidney of a 3. Cold ischemic time for the allograft was 1. She had oliguria in the first 3 h of surgery with urine output of 1. Although BP was 1. Hg, CVP was low, 25 cm H2. O. She received three boluses of normal saline, which was followed by a prompt increase in rate of UOP to 1. Blood urea nitrogen was 4. L, while serum Cr was 1. L shortly after the graft surgery. By post operative day 3, serum creatinine had decreased to 7. L while by the 7th day the Cr was 1.
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