It has long been known that the kidney, in its functioning state, is distended with blood (1-4). Rose-Bradford (1) stressed the "passive" character of this distension, for he noted that the kidney swelled when the blood pressure rose and shrank when it fell. Text- fig. 1 shows how the organ collapses when its circulation is abruptly cut off; in this instance, although drainage was obviously incomplete, it shrank from a volume of 49 cc. to a volume of 39 cc., showing that at least 20 per cent of its normal functioning volume was distending fluid. This fluid drains from the renal vein when the renal artery is occluded; in quantity, when drainage is complete, it averages 26 per cent of the functionally distended kidney (5, 6).This aspect of renal behavior has, however, been overlooked by those investigating the functional vascular morphology of the organ. Led recently by Trueta el al. (7), many studies of blood distribution have been attempted, using particularly the technic of injecting India ink into the vascular system and then, at necropsy, examining the distribution of ink. In such studies, the distribution of ink at necropsy should reflect the distribution while the organ is functioning. But if the kidney's blood were to drain out after removal, the subsequent localization of the dye would give only very rough information about the distribution of blood in the functioning organ. The latter is not thoroughly known and hence the present study was undertaken.Actually, the fluid naturally distending the kidney is not blood alone; rather, it is a fluid containing less red cells and less plasma protein than simultaneously drawn blood, the same amount of Na and Ca, and increased quantities of K, C1, urea, and PO4 (6). Because kidney interstitial fluid (or lymph) has approximately this same composition, we have concluded that the distending fluid is very probably a mixture of blood and interstitial fluid. Furthermore, since the distending fluid contains only about half the red cells that blood contains (6), the volume of its two components, in terms of percentage of the functionally distended kidney, is 13 per cent blood and 13 per cent interstitial fluid.
Introduction - The combination of sodium glucose cotransporter-2 inhibitor (SGLT-2i) use and glucocorticoid excess can trigger ketone production by reducing insulin secretion/sensitivity and stimulating glucosuria, glucagon production, and lipolysis. In addition, metabolic alkalosis caused by glucocorticoid excess (via mineralocorticoid receptor activation) may combine with diabetic ketoacidosis (DKA) to create a mixed acid-base disorder, which can potentially obscure SGLT-2i-associated DKA. Case Description - A 45 year-old man with well-controlled type 2 diabetes on an SGLT-2i presented to the Emergency Room with edema, weakness, palpitations, polyuria/polydipsia, hypertension, and hyperglycemia. Exam was significant for a blood pressure of 195/111mmHg, moon facies, supraclavicular fat pad fullness, obese abdomen with violaceous striae, and reduced bilateral hip flexor weakness. He was found to have potassium 2.5mmol/L, glucose 296mg/dL, bicarbonate 28mmol/L, and anion gap 20mmol/L. Venous pH was 7.51, with pCO2 38mmHg. Beta-hydroxybutyrate was >8.0mmol/L (<0.40). Random cortisol was 59.1ug/dL (5-25ug/dL) and ACTH 313pg/mL (15-66pg/mL). 24hr Urine Cortisol was 1567mcg/24hrs (3.5-45mcg/24hrs). Pituitary MRI showed diffuse pituitary enlargement and a 7mm pituitary adenoma. The patient’s DKA was managed with IV fluids and insulin, and potassium was aggressively replaced. He underwent successful trans-sphenoidal pituitary adenoma resection, with positive ACTH staining on pathology. ACTH and cortisol 12 hours postoperatively were 78pg/mL and 15.1ug/dL, respectively, and continued to downtrend. On the second postoperative day, the patient developed severe anxiety, which improved with increased glucocorticoid supplementation. Conclusion - DKA is a rare side effect of SGLT-2i use, and even rarer in the setting of Cushing’s Disease. In this case, the patient’s underlying Cushing’s Disease likely contributed to the development of SGLT-2i-associated DKA and severe hypokalemia, while also obscuring the diagnosis by causing a concurrent metabolic alkalosis that normalized the pH and bicarbonate. The competing physiologic mechanisms at play led to this unusual presentation of SGLT-2i-associated DKA with an alkalotic pH and normal bicarbonate.
Background Hypercalcemia of malignancy is typically associated with bony metastases or production of PTHrP. However, rarely, it can be due to intact PTH (iPTH) secretion from solid tumors 1 . Clinical Case A 61 year old man with chronic kidney disease and hepatitis C cirrhosis complicated by hepatocellular carcinoma (HCC) presented with abdominal pain and was found to have hypercalcemia and a new 5 cm mesenteric mass. Admission labs showed PTH-mediated hypercalcemia: calcium 12.7 mg/dl (8.5-10.1 mg/dl), albumin 3.1 g/dl (3.5-4.8 g/dl), serum creatinine 2.4 mg/dl (0.6-1.4 mg/dl), PTH 397.4 pg/ml (18.4-88 pg/ml), PTHrP 16 (14-27 pg/ml), 25-OH Vitamin D 12.9 ng/ml (30-100 ng/dl), and 1,25-OH Vitamin D 12 (18-72 pg/ml). SPEP and UPEP were normal. Prior to presentation, his baseline calcium was normal and PTH had ranged 150-180 pg/ml with similar renal function as on admission. A parathyroid ultrasound and sestamibi scan were negative for a parathyroid adenoma. A nuclear bone scan was negative for bony metastases. An octreotide scan was also negative. A PET-CT scan showed an FDG-avid mesenteric mass and new FDG-avid hepatic lesions. A biopsy of the mesenteric mass was consistent with metastatic HCC and stained positive for PTH, which suggested iPTH secretion from the HCC. The patient was given IV fluid, calcitonin and cinacalcet with minimal improvement in his hypercalcemia. He later received pamidronte and also underwent embolization to one of the larger hepatic HCC lesions. The mesenteric HCC lesion was not resectable, nor was it amendable to embolization. His calcium normalized after treatment, though his PTH remained very elevated, indicating this improvement was from the pamidronate and not the embolization. Hypercalcemia in other reported cases of iPTH secretion from HCC did improve after embolization 2,3 , though in these cases, the HCC had not metastasized. The patient had several recurrent admissions for hypercalcemia with increasingly poor response to bisphosphonates. His PTH had climbed to 1275 pg/ml. Denosumab therapy was considered, but he had transitioned to hospice care and died 3 months after his initial presentation. Conclusion Intact PTH secretion from HCC is a rare cause of hypercalcemia References 1. Kandil E, Noureldine S, Kalek MA et al. Ectopic secretion of parathyroid hormone in a neuroendocrine tumor: a case report and review of the literature. Int J Clin Exp Med. 2011:4(3):234-40. 2. Abe Y, Makiyama H, Fujita Y, et al. Severe hypercalcemia associated with hepatocellular carcinoma secreting intact parathyroid hormone: a case report. Intern Med. 2011;50(4):329-33. 3. Koyama Y, Ishijima H, Ishibashi A, et al. Intact PTH-producing hepatocellular carcinoma treated by transcatheter arterial embolization. Abdom Imaging 24: 144-146, 1999.
Background: Kallman Syndrome (Isolated gonadotropin-releasing hormone (GnRH) deficiency with anosmia/hyposmia) affects both sexes but has male preponderance. The sex difference likely relates to genetics and possible early diagnosis in males because of microphallus and cryptorchidism. The presentation of Kallman syndrome in females may be very subtle and may lead to a delay in the diagnosis and management. Clinical Case A 62-year-old Caucasian female with a history of hypertension, hyperlipidemia, seizure disorder, COPD, multiple fractures and peripheral vascular disease was referred for evaluation of chronic hyponatremia that was diagnosed 6 years ago. The patient was euvolemic on the exam, and laboratory evaluation was consistent with SIADH. Labs showed Na 122-130 mmol/L, normal thyroid function and cortisol levels, serum Osm 259 mOsm/kg (Normal 280-300 mOsm/kg), urine Osm 565mOsm/kg (Normal 50-1200 mOsm/kg). Hyponatremia had been managed with fluid restriction and salt tablets. Other work-up was negative for malignancy. Unrelated to hyponatremia, the patient had striking virilization and hirsutism. On further history, she reported primary amenorrhea, infertility, lack of secondary sexual characteristics and anosmia. Physical exam was notable for absent secondary female sexual characteristics. Additional family history revealed a brother with anosmia and incomplete secondary sexual development and multiple females who never achieved puberty or fertility. Further workup included a normal pituitary MRI, and inappropriately low FSH of 1.0mIU/ml and LH of 0.3 m IU/ml (expected post-menopausal levels > 51 and 14, respectively). Other pituitary axis evaluation was normal. The patient also had a history of low trauma fractures of the hip and forearm. Bone density scan showed severe osteoporosis with a T-Score of -4.80 at the right femoral neck and -4.90 at the spine. Secondary osteoporosis work-up was negative. She was started on anabolic therapy with Teriparatide with plans to follow with antiresorptive therapy. Conclusion: This patient was diagnosed with hypogonadotropic hypogonadism due to Kallman Syndrome with severe osteoporosis. This case illustrates the value of physical exam and considering diagnoses and work up beyond the initial reason for consultation. A timely diagnosis in her case could have improved her quality of life, helped her achieve fertility and possibly may have prevented severe osteoporosis. The literature review also suggests a significant percentage of patients do not receive treatment for osteoporosis after hip fracture. (1) References 1 -Solomon DH, Johnston SS, Boytsov NN, McMorrow D, Lane JM, Krohn KD. Osteoporosis Medication Use After Hip Fracture in U.S. Patients Between 2002 and 2011, J Bone Miner Res. 2014 Sep;29(9):1929-37.
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