Abstract: Methods and systems are provided for integrated genomic analysis of chronic kidney disease (CKD) genes and pharmacogenomic genes in a human subject. A biological sample is obtained from the subject and genomic DNA is extracted from the sample. Genomic regions of one or more CKD genes and pharmacogenomic genes are simultaneously amplified using a multiplex primer pool. Amplified DNA fragments are used to prepare a sequencing library and are sequenced using a next-generation sequencing platform. Sequencing reads are processed by a computer processor to align the reads to a reference genome and identify sequence variants within the amplified genomic regions. Output data identifying detected sequence variants are generated for use in clinical evaluation and management of the subject. In some implementations, the genomic variant data are used to guide pharmacological treatment selection or drug dosage for the subject based on detected pharmacogenomic variants.

Abstract: A method for determining a subject's risk for developing chronic kidney disease (CKD) combined with determining a subject's pharmacogenomic (PGX) profile is described. The method involves obtaining a sample of genetic material from the subject. The genetic material is amplified using primers specific for the genes underlying CKD and PGX. The DNA sequence of the amplified genetic material is determined and compared with the human reference genome sequence. One or more DNA sequence alterations in the amplified genetic material not present in the human reference genome sequence determines the PGX profile of the subject and may indicate that the subject is at risk for developing CKD.

Abstract: A method for determining a subject's risk for developing hemophilia A, hemophilia B, or von Willebrand disease (VWD) is described. The method involves obtaining a sample of genetic material from the subject. The genetic material is amplifed using primers specific for the genes underlying hemophilia A, hemophilia B and VWD. The DNA sequence of the amplified genetic material is determined and compared with a DNA sequence from a normal control subject. One or more DNA sequence alterations in the amplified genetic material not present in the DNA sequence from the normal control subject indicates that the subject is at risk for developing hemophilia A, hemophilia B, or VWD.

Abstract: The present invention is directed to a method of diagnosing infection with SARS-CoV-2. The method involves first obtaining a sample from a patient, followed by the use of a mobile testing laboratory to test the sample for SARS-CoV-2 nucleic acid. The sample is tested by extracting the RNA from the patient sample, amplifying the nucleic acid using reverse transcription loop-mediated isothermal amplification (RT-LAMP), and measuring the results. Results from the RT-LAMP are obtained within 60 minutes after sample collection, where a positive result is indication of infection with SARS-CoV-2.

Abstract: A method for determining a subject's risk for developing hemophilia A, hemophilia B, or von Willebrand disease (VWD) is described. The method involves obtaining a sample of genetic material from the subject. The genetic material is amplified using primers specific for the genes underlying hemophilia A, hemophilia B and VWD. The DNA sequence of the amplified genetic material is determined and compared with a DNA sequence from a normal control subject. One or more DNA sequence alterations in the amplified genetic material not present in the DNA sequence from the normal control subject indicates that the subject is at risk for developing hemophilia A, hemophilia B, or VWD.

Abstract: A method for identifying a patient's risk for developing complement-mediated thrombic microangiopathy is described. A sample of genetic material is obtained from a patient. The genetic material is amplified using primers specific for complement-mediated thrombic microangiopathy. After amplification, the genetic sequence of the amplicon is determined. The genetic sequence of the amplicon is compared to a reference sequence, and variations are identified between the sample amplicon and the reference sequence. A variation between the sample amplicon and the reference sequence is indicative of a risk for the patient for developing complement-mediated thrombic microangiopathy.

Abstract: A method for identifying a patient's risk for developing complement-mediated thrombic microangiopathy is described. A sample of genetic material is obtained from a patient. The genetic material is amplified using primers specific for complement-mediated thrombic microangiopathy. After amplification, the genetic sequence of the amplicon is determined. The genetic sequence of the amplicon is compared to a reference sequence, and variations are identified between the sample amplicon and the reference sequence. A variation between the sample amplicon and the reference sequence is indicative of a risk for the patient for developing complement-mediated thrombic microangiopathy.