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Ageing
Published in Henry J. Woodford, Essential Geriatrics, 2022
Co-existing hypertension or diabetes may accelerate renal function loss. A reduction in muscle mass means that serum creatinine concentration may change little despite this declining function, which may make it hard to estimate GFR. Decreased renal reserve and concentrating ability reduce our capacity to compensate for fluid or electrolyte imbalances. There is an increased risk of nephrotoxicity from drugs or radiocontrast agents. Proteinuria is not a feature of normal ageing. A larger proportion of urine is formed at night (see page 257). The bladder becomes less elastic due to increased collagen deposition, which leads to reduced distension and impaired emptying abilities.
The patient with acute renal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
This is when actual structural damage to the nephrons has occurred and it may lead to acute tubular necrosis, where tubular cells die and are shed into the tubule lumen, resulting in tubular blockages. The most common causes for this are as follows:Prolonged hypoperfusion.Nephrotoxic drug therapy, especially the aminoglycoside antibiotics and the non-steroidal anti-inflammatory agents.Exposure to radiocontrast agents.Infections, for example unresolved glomerulonephritis.Other diseases that can affect tubular function, such as sickle-cell disease and certain malignancies.
Drug-induced thyroid dysfunction
Published in David S. Cooper, Jennifer A. Sipos, Medical Management of Thyroid Disease, 2018
Victor Bernet, Robert C. Smallridge
Medications known to reduce T4 to T3 conversion include amiodarone, glucocorticoids, gallbladder dyes, such as ipodate and iopanoic acid and propranolol and nadolol in high doses, and propylthiouracil. Amiodarone inhibits T4 5¢-monodeiodination which can lead to a rise in serum T4 and rT3, a concomitant decline in serum T3, and a secondary rise in serum TSH levels (96). These changes typically resolve within 3-6 months of initiation of therapy or with discontinuation of amiodarone. If the serum TSH remains elevated after more than 3–6 months, the patient can be considered to have amiodarone-induced hypothyroidism. If amiodarone needs to be continued, treatment with levothyroxine should be initiated, but levothyroxine doses needed to normalize serum TSH levels may be higher than expected due to inhibition of T4 to T3 conversion as previously discussed (97). The radiocontrast agents ipodate and iopanoic acid also inhibit T4 to T3 conversion, but are no longer available in the United States (98).
Is the combination of linagliptin and allopurinol better prophylaxis against post-contrast acute kidney injury? A multicenter prospective randomized controlled study
Published in Renal Failure, 2023
Ahmed Fayed, Ahmed A. Hammad, Dina O. Abdulazim, Hany Hammad, Mohamed Amin, Samir Elhadidy, Mona M. Salem, Ibrahim M. Abd ElAzim, Lajos Zsom, Eva Csongradi, Karim M. Soliman, Usama A. Sharaf El Din
The primary endpoint was the development of post-contrast AKI, defined as a decrease of GFR by or greater than 30% relative to baseline or an increase in serum creatinine that is greater than 0.3 mg/dl relative to baseline or 30% over baseline 72 h after the administration of the contrast. A secondary endpoint was the maximum absolute change in serum creatinine and GFR during the study period. GFR was estimated using the MDRD 4-variable GFR Equation (GFR in mL/min per 1.73 m2 = 175 x SerumCr−1.154 x age−0.203 x 1.212 (if the patient is black) x 0.742 (if female)). Table 2 summarizes the different radiologic procedures performed as well as the types and amounts of radiocontrast agents used. Change in any of the studied parameters was calculated as a change in percentage [{(post-level-basal level)/basal level} X 100].
Cranial Polyneuropathy Secondary to Remote Iophendylate Myelography
Published in Neuro-Ophthalmology, 2022
Radiocontrast agents are invaluable substances that not only enhance the visibility of internal structures but also offer diagnostic direction. Their use in neuroradiology can be found as early as 1918 with the development of ventriculography and pneumoencephalography by Dr Walter Dandy, cerebral angiography in 1930 by Dr Egas Moniz, and myelography with iophendylate in 1944.1,2 Today, contrast media are used most often with magnetic resonance imaging (MRI), computed tomography (CT), and catheter angiography, with well-known adverse reactions including nephrogenic systemic fibrosis, anaphylactoid reactions, and contrast nephropathy. Although rare, side effects may manifest years after use, especially with poorly absorbed contrast agents. I report a case of iophendylate-induced inflammation causing a cranial polyneuropathy, including a left trochlear nerve paresis and left trigeminal sensory neuropathy, about 30 years after myelography.
Biomarker evidence for distal tubular damage but cortical sparing in hospitalized diabetic patients with acute kidney injury (AKI) while on SGLT2 inhibitors
Published in Renal Failure, 2020
Said Darawshi, Hiba Yaseen, Yuri Gorelik, Caroline Faor, Auryan Szalat, Zaid Abassi, Samuel N. Heyman, Mogher Khamaisi
The outer medulla is physiologically hypoxic, the consequence of limited regional blood and oxygen supply, combined with intense oxygen consumption for tubular transport, carried out chiefly by medullary thick ascending limbs (mTALs) [18]. In anesthetized rats SGLT inhibition decreases proximal tubular transport, leading to improved cortical pO2. By contrast, medullary physiologic hypoxia intensifies, likely due to increased solute delivery to distal nephron segments, enhancing medullary tubular transport work and oxygen consumption [19]. Indeed, Dapagliflozin enhanced Hypoxia-Inducible Factor (HIF) expression in mice kidneys, reflecting reduced tissue oxygenation [20]. In humans, SGLT2i increased plasma erythropoietin and induced reticulocytosis [21], likely reflecting intensified hypoxia at the corticomedullary junction [22]. Thus, it is tempting to assume that while hypoxic injury might be mitigated in cortical tissues in patients treated with SGLT2i, hypoxic medullary injury may develop, particularly when mechanisms that match regional blood flow and tubular transport are hampered, or in the presence of additional conditions that alter medullary oxygenation (such as CKD, diabetes or aging) [18,23]. Indeed, the diabetic kidney is especially prone to hypoxic medullary injury, as outlined in detail elsewhere [24]. This has led us to propose the avoidance of concomitant use of NSAIDs and to discontinue SGLT2i before the administration of iodine-based radiocontrast agents [25], since these interventions are characterized by significant intensification of medullary hypoxia [26].